Topical taurine, anyone tried?

Joined
Nov 16, 2012
Messages
761
Has anyone attempted topical taurine as a potential hair loss treatment?

Research has led me to the significance of TGF-beta as a driver of fibrosis and one of the major factors implicated in baldness, and after seeing this study where taurine basically counteracts that extremely successfully, I am inclined to use it:


Seriously, those kinked hairs as seen in the study, are coming off of my head on a daily basis.

I have attempted to use 1% so far, but immediately I noticed being really tired since I started using it. I will get random yawning spells throughout the day and just be sleepy as hell and low energy.
I've since switched to 0.1% since according to the studies a large concentration isn't necessary. And this has only marginally improved the side effects.

My hair feels healthier since using it and I think that long-term it would have strong potential to severely slow down if not stop baldness, but I don't know if there's a way to get around this sleepiness and tiredness or why in particular taurine would cause that. It is even more ridiculous since at 0.1% you are only getting like 2-3 mg of taurine into the bloodstream at best, yet I used to take 1-2 g orally and had no such issues (but I also didn't get the feeling it was effective for hair).
 

md_a

Member
Joined
Aug 31, 2015
Messages
297
I think there are several ways in which taurine could help with hair loss. I haven't tested it yet, I was just curious to read about it. A possible mechanism for improving the quality of hair by taurine is inhibition of the renin angiotensin aldosterone system, regulation of intracellular calcium, prevention of excess collagen, anti-fibrotic and anti-stress (adrenal hyperactivity) and many other ways.

...

The Wnt/β-catenin pathway is known to positively affect mammalian HF growth and cycling (Andl et al., 2002; Ito et al., 2007). After activation, β-catenin accumulates in the cytoplasm and then translocates to the nucleus, where it interacts with Lef/Tcf transcription factors to regulate the expression of genes responsible for HF growth. The activity of β-catenin, the key molecule in the Wnt/β-catenin pathway, can be suppressed by glycogen synthase kinase-3β (GSK-3β), which is inhibited by phosphorylation. DHT abrogates the ability of dermal papilla cells (DPCs) from patients with AGA to induce HF stem cell differentiation via inhibition of the Wnt/β-catenin pathway in DPCs, which involves inhibiting GSK-3β activity (Mulholland et al., 2005). Therefore, we hypothesized that the Wnt/β-catenin pathway is essential to HF growth regulation by DHT.

The present study shows that the impact of DHT on HF growth and cycling varies at different concentrations by interacting with the Wnt/β-catenin signaling pathway.
We provide evidence that activation of the Wnt/β-catenin pathway can weaken the negative influence of high-dose DHT on HFs.

Dihydrotestosterone Regulates Hair Growth Through the Wnt/β-Catenin Pathway in C57BL/6 Mice and In Vitro Organ Culture

.....

Dickkopf 1 promotes regression of hair follicles​

Abstract​

Recently, we suggested that Dickkopf 1 (DKK-1) is a pathogenic mediator involved in male pattern baldness. As premature catagen onset is a key characteristic of male pattern baldness, in this study, we evaluated whether DKK-1 has a role as a catagen inducer in hair cycling. Herein, we report that recombinant human DKK-1 (rhDKK-1) injection into the hypodermis of mice during anagen caused premature onset of catagen, whereas neutralizing DKK-1 antibody delayed anagen-to-catagen transition in mice. Moreover, treatment with rhDKK-1 led to a decrease in final hair follicle length, whereas DKK-1 antibody led to an increase compared with control animals. In addition, DKK-1 and DKK-1 messenger RNA expression is most upregulated in follicular keratinocytes of late anagen in depilation-induced hair cycle progression. Moreover, we observed that rhDKK-1 blocks canonical Wnt-mediated activation of β-catenin signaling and induces the proapoptotic protein Bax, resulting in apoptosis in outer root sheath keratinocytes. Taken together, our data strongly suggest that DKK-1 is involved in anagen-to-catagen transition in the hair cycle by regulating the activity of follicular keratinocytes.

Dickkopf 1 promotes regression of hair follicles - PubMed



Oxidative stress management in the hair follicle: Could targeting NRF2 counter age-related hair disorders and beyond?​

Abstract​

Widespread expression of the transcription factor, nuclear factor (erythroid-derived 2)-like 2 (NRF2), which maintains redox homeostasis, has recently been identified in the hair follicle (HF). Small molecule activators of NRF2 may therefore be useful in the management of HF pathologies associated with redox imbalance, ranging from HF greying and HF ageing via androgenetic alopecia and alopecia areata to chemotherapy-induced hair loss. Indeed, NRF2 activation has been shown to prevent peroxide-induced hair growth inhibition. Multiple parameters can increase the levels of reactive oxygen species in the HF, for example melanogenesis, depilation-induced trauma, neurogenic and autoimmune inflammation, toxic drugs, environmental stressors such as UV irradiation, genetic defects and aging-associated mitochondrial dysfunction. In this review, the potential mechanisms whereby NRF2 activation could prove beneficial in treatment of redox-associated HF disorders are therefore discussed.

Oxidative stress management in the hair follicle: Could targeting NRF2 counter age-related hair disorders and beyond? - PubMed

….

In the present study, we found that taurine significantly increased the expression of β-catenin and that the protective effects induced by taurine are partially eliminated by a Wnt/β-catenin signaling inhibitor (i.e., DKK1). Interestingly, the inhibition of β-catenin by DKK1 not only led to elevated oxidative stress and reduced ALP but also caused the decreased expression of ERK, compared to taurine-treated cells. These results suggest that taurine inhibits oxidative stress-induced apoptosis and promotes osteoblast mineralization by activating the Wnt/β-catenin signaling pathway. More importantly, we found that Wnt/β-catenin signaling can regulate ERK phosphorylation, thereby increasing antioxidant response to oxidative stress.

Our findings indicate that taurine activates Nrf2, induces the expression of antioxidant enzymes (i.e., NQO1, HO1, and GCLC), and reduces H2O2-induced cell death by activating ERK and the Wnt/β-catenin pathway in osteoblast cells. Considering the partial reduction of ERK, antioxidants, and ALP activities by DKK1, a Wnt/β-catenin inhibitor, it is possible that other signaling molecules and pathways could be involved (Fig. 5). Thus, to explore other pathways that likely participate in taurine-mediated antioxidant effects, such as the PI3K/AKT signaling pathway (Jang et al., 2016), further research is necessary.

Cytoprotective Effect of Taurine against Hydrogen Peroxide-Induced Oxidative Stress in UMR-106 Cells through the Wnt/β-Catenin Signaling Pathway
.............

The site of taurine uptake, i.e. the hair bulb, is an area where a highly active cellular proliferation takes place, one of the most active in the whole body and from which all different follicular compartments originate [36]. This compartment is structurally and functionally surprisingly stable, since, when grown in a totally defined medium, isolated hair follicle keeps producing a normal hair fibre [18, 37]. Moreover, survival rate in vitro is increased when isolated human hair follicles are grown in the presence of taurine. These findings strongly suggest that taurine could be involved in the maintenance of human hair bulb either as an osmolyte [4, 13, 14, 38] or a regulator of cysteine and/or calcium metabolism [35].

Alternatively, it is now well established that during the development of androgenetic alopecia and the progressive transformation of terminal into vellus‐like follicles, inflammatory events occur that precede perifollicular fibrosis and ultimately sclerosis of collagenous streamers [15-17]. In this respect, taurine was described as a protective agent against age‐related progressive renal fibrosis in rats [39]. As one of the master switches of the fibrotic program is TGF‐β1, a growth factor known to inhibit hair growth in vitro [19], and since taurine can inhibit collagen synthesis [9], a down‐stream response to TGF‐β1 [40], we further investigated a possible protective role of taurine against TGF‐β1‐induced alterations. Interestingly, the most conspicuous effect of TGF‐β1 treatment was the curvature of hair follicle bulb, accompanied by a thickening of the dermal sheath as demonstrated by collagen staining. In fact, this phenomenon likely resulted from combined dermal sheath myofibroblast activation [41] and inhibition of matrix keratinocyte proliferation [19, 42, 43]. Taurine treatment dramatically counteracted this effect through a biological mechanism which remains to be explained.

Error - Cookies Turned Off

..........

Simulative evaluation of taurine against alopecia caused by stress in Caenorhabditis elegans​

Abstract​

Hair loss or alopecia has been portrayed as a modern malady which is aggravated by stressful conditions. Major cases of alopecia were found among individuals of 40s-50s, nowadays, even among the 20s-30s. This study characterized taurine's potential against alopecia caused by chemical stress agents based on the comparison with other commercially available anti-alopecia agents using Caenorhabditis elegans. The criteria used are their effects on the expression of stress markers and measurements of vital signs: lifespan comparison, progeny number, and mobility. C. elegans showed the typical stress symptoms under treatment with tunicamycin, endoplasmic reticulum stress agent. Hsp-70 protein expression increased, while worm's lifespan and per capita progeny number significantly decreased along with an unusually retarded movement. A positive response was shown when worms were treated with taurine along with astressin-B and finasteride. Between the treatments, finasteride showed better outcomes in terms of stress-reducing effects. Taurine helped worms recover more effectively from adverse influence of stress. In conclusion, there is strong evidence that taurine has a great potential as anti-alopecia effect especially against the one caused by the chemical stress. The present study implies that taurine might strongly work against hair loss when used in combination with other commercially available -anti-alopecia agents.

Simulative evaluation of taurine against alopecia caused by stress in Caenorhabditis elegans - PubMed

............

The mechanisms of taurine mediated protection against cell damage induced by hypoxia and reoxygenation

Abstract

Taurine administered during hypoxia markedly reduced the cell damage due to O2 deficiency and reoxygenation. Different mechanisms are responsible for the improved survival of the renal cell cultures. Taurine markedly reduces the osmoregulatory deterioration during hypoxia and reoxygenation. Calcium homeostasis was markedly improved. Ca2+ efflux during hypoxia as well as Ca2+ overload during reoxygenation was significantly reduced by the amino acid. The effect of taurine was partly comparable to the effect induced by Ca2+ channel blockers. One of the effects mainly responsible for cellular protection seems to be the taurine-induced acceleration of cellular growth processes in spite of hypoxia and reoxygenation. The spectrum of cytoprotective effects of taurine predisposes this substance to be a physiological protective agent responsible for cellular homeostasis or enantiostasis.

The mechanisms of taurine mediated protection against cell damage induced by hypoxia and reoxygenation - PubMed

.............

Interaction between the actions of taurine and angiotensin II

Abstract

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.

Interaction between the actions of taurine and angiotensin II - PubMed


................

Effects of Taurine on ACE, ACE2 and HSP70 Expression of Hypothalamic-Pituitary-Adrenal Axis in Stress-Induced Hypertensive Rats​

Abstract​

The experiment was to elucidate protective mechanism of taurine against stress-induced hypertension. Thirty two male Wistar rats were randomly divided into four groups. Normal control group and stress control group were intragastrically administered saline; β-alanine stress group were fed with β-alanine (200 mg/kg/day) and taurine stress group with taurine (200 mg/kg/day). The hypertensive model was established by giving rats stress for 3 weeks.Results showed that significant expression levels of angiotensin converting enzyme (ACE) in the hypothalamus, pituitary and adrenal were observed in β-alanine stress group and stress control group (P < 0.05), but significant mRNA expression levels of angiotensin-converting enzyme 2 (ACE2) in taurine stress group and normal control group (P < 0.05). All the groups showed no significant differences in HSP70 mRNA expression levels in hypothalamus (P > 0.05), while taurine stress group exhibited the highest HSP70 mRNA expression levels both in pituitary and in adrenal (P < 0.05). It was also found that β-alanine stress group and stress control group had significantly higher protein expression levels of ACE in hypothalamus, pituitary and adrenal (P < 0.05), but significantly lower protein expression of ACE2 compared to taurine stress group and control groups (P < 0.05). The results indicated that taurine regulated the hypothalamus pituitary adrenal (HPA) axis of the renin-angiotensin-aldosterone system (RAAS) by inhibiting ACE gene and protein expressions and promoting ACE2 and HSP70 protein expressions, thereby contributing to the prevention of stress-induced hypertension.

Effects of Taurine on ACE, ACE2 and HSP70 Expression of Hypothalamic-Pituitary-Adrenal Axis in Stress-Induced Hypertensive Rats - PubMed

.............

Effects of Taurine on Blood Index of Hypothalamic Pituitary Adrenal (HPA) Axis of Stress-Induced Hypertensive Rat​

Abstract​

To elucidate the protective mechanism of taurine against stress induced hypertension, 32 male Wistar rats were randomly divided into four groups: normal control group; stress control group; β–alanine stress group and taurine stress group. Rats of the two control groups were administered physiological saline while the β–alanine treated group was administered β–alanine (200 mg/kg/day) and the taurine treated group was administered taurine (200 mg/kg/day). The hypertensive model was produced by stressing the rats for 3 weeks. Serum levels of angiotensin converting enzyme (ACE), angiotensin II (AngII), glucocorticoid hormone (CRH), adrenocorticotropic hormone (ACTH), Glucocorticoid (GC), epinephrine (EPI), norepinephrine (NA) in the β–alanine stress group was significantly higher than those of the other groups (P < 0.05). However, serum of the taurine stress group contained more angiotensin converting enzyme 2 (ACE2) than those of the other groups (P < 0.05). These data indicate that taurine regulates the hypothalamus pituitary adrenal (HPA) axis of the renin-angiotensin-aldosterone system (RAAS), thereby contributing to the prevention of stress-induced hypertension.

Effects of Taurine on Blood Index of Hypothalamic Pituitary Adrenal (HPA) Axis of Stress-Induced Hypertensive Rat

..........

Effect of taurine on alteration in adrenal functions induced by stress

Abstract

When rats were exposed to immobilized cold stress, adrenaline content in the adrenal gland as well as noradrenaline content in the brain stem were reduced drastically, while noradrenaline content in the atria was not altered by the application of stress. Oral administrations of taurine (4-7 g/kg/day, for 3 days) prevented the stress-induced decline of adrenaline in the adrenal gland and this preventive effect could not be duplicated by the administration of L-isoleucine or DL-methionine. In hypophysectomized rats, the stress also induced a significant fall in adrenaline content of the adrenal gland, however taurine administration did not show significant preventive effects on the decline in adrenal catecholamines. The immobilized cold stress induced a significant increase in blood sugar and this increase was antagonized by pretreatment with taurine. Taurine had no significant effects on the stress-induced increase in the activity of adrenal tyrosine hydroxylase and the turnover rate of adrenaline in the adrenal gland measured by the rate of decline of this amine following alpha-methyl-tyrosine administration. The administration of taurine, in both in vivo and in vitro, inhibited the release of adrenaline from adrenal medullary granules, but that of dopamine-beta-hydroxylase was not significantly affected. The stress-induced elevation of the blood level of corticosterone was not affected by taurine administration. These findings indicate that taurine antagonizes the stress-induced elevation of blood sugar by reducing adrenaline output from the adrenal gland. The regulatory mechanism most likly involves the inhibition of adrenaline release from adrenal medullary granules, possibly by stabilizing the membrane of the granules.

Effect of taurine on alteration in adrenal functions induced by stress - PubMed

......

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease​

Abstract​

Taurine is a non-protein amino acid that is expressed in the majority of animal tissues. With its unique sulfonic acid makeup, taurine influences cellular functions, including osmoregulation, antioxidation, ion movement modulation, and conjugation of bile acids. Taurine exerts anti-inflammatory effects that improve diabetes and has shown benefits to the cardiovascular system, possibly by inhibition of the renin angiotensin system. The beneficial effects of taurine are reviewed.

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease - PubMed

................

Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons​

Abstract​

Glutamate-induced excitotoxicity has been implicated as an important mechanism underlying a variety of brain injuries and neurodegenerative diseases. Previously we have shown that taurine has protective effects against glutamate-induced neuronal injury in cultured neurons. Here we propose that the primary underlying mechanism of the neuroprotective function of taurine is due to its action in preventing or reducing glutamate-induced elevation of intracellular free calcium, [Ca(2+)](i). This hypothesis is supported by the following findings. First, taurine transport inhibitors, e.g., guanidinoethyl sulfonate and beta-alanine, have no effect on taurine's neuroprotective function, suggesting that taurine protects against glutamate-induced neuronal damage through its action on the extracellular membranes. Second, glutamate-induced elevation of [Ca(2+)](i) is reduced to the basal level upon addition of taurine. Third, pretreatment of cultured neurons with taurine prevents or greatly suppresses the elevation of [Ca(2+)](i) induced by glutamate. Furthermore, taurine was found to inhibit the influx but not the efflux of (45)Ca(2+) in cultured neurons. Taurine has little effect on the binding of [(3)H]glutamate to the agonist binding site and of [(3)H]MDL 105,519 to the glycine binding site of the N-methyl-D-aspartic acid receptors, suggesting that taurine inhibits (45)Ca(2+) influx through other mechanisms, including its inhibitory effect on the reverse mode of the Na(+)/Ca(2+) exchangers (Wu et al. [2000] In: Taurine 4: taurine and excitable tissues. New York: Kluwer Academic/Plenum Publishers. p 35-44) rather than serving as an antagonist to the N-methyl-D-aspartic acid receptors.

Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons - PubMed

............

Taurine increases mitochondrial buffering of calcium: role in neuroprotection

Abstract

We have determined the role of mitochondria in the sequestration of calcium after stimulation of cerebellar granule cells with glutamate. In addition we have evaluated the neuroprotective role of taurine in excitotoxic cell death. Mitochondrial inhibitors were used to determine the calcium buffering capacity of mitochondria, as well as how taurine regulates the ability of mitochondria to buffer intracellular calcium during glutamate depolarization and excitotoxicity. We report here that pre-treatment of cerebellar granule cells with taurine (1 mM, 24 h) significantly counteracted glutamate excitotoxicity. The neuroprotective role of taurine was mediated through regulation of cytoplasmic free calcium ([Ca(2+)]( i )), and intra-mitochondrial calcium homeostasis, as determined by fluo-3 and (45)Ca(2+)-uptake. Furthermore, the overall mitochondrial function was increased in the presence of taurine, as assessed by rhodamine accumulation into mitochondria and total cellular ATP levels. We specifically tested the hypothesis that taurine reduces glutamate excitotoxicity through both the enhancement of mitochondrial function and the regulation of intracellular (cytoplasmic and intra-mitochondrial) calcium homeostasis. The role of taurine in modulating mitochondrial calcium homeostasis could be of particular importance under pathological conditions that are characterized by excessive calcium overloads. Taurine may serve as an endogenous neuroprotective molecule against brain insults.

Taurine increases mitochondrial buffering of calcium: role in neuroprotection - PubMed

......

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus​

Abstract​

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus.

Background: Knowledge about biological functions of podocytes in the glomerulus is limited because of its unique anatomical location. Here we introduce a new method for measuring the intracellular calcium activity ([Ca2+]i) in the podocyte in the intact glomerulus.

Methods: With the help of fluorescence high-resolution digital imaging and a recently developed ultraviolet laser-scanning microscope, [Ca2+]i was measured in fura-2-loaded glomeruli and single podocytes of intact microdissected rat glomeruli.

Results: Angiotensin II (Ang II) increased [Ca2+]i reversibly in a biphasic and concentration-dependent manner. In contrast to Ang II, bradykinin, thrombin, arginine vasopressin, and serotonin did not change [Ca2+]i in the glomerulus. At reduced extracellular Ca2+ activity, Ang II released [Ca2+]i from intracellular stores, but the second phase, corresponding to a Ca2+ influx from the extracellular space, was absent. The L-type Ca2+ channel blocker nicardipine did not influence the Ang II-mediated [Ca2+]i increase, and an increase of the extracellular K+ concentration did not change [Ca2+]i in the glomerulus. The angrotensin II type I (AT1) receptor antagonist losartan inhibited the Ang II-mediated [Ca2+]i increase. Confocal [Ca2+]i measurements using fura-2 or fluo-3 or fluo-4 on the single cell level show that some of the Ang II-mediated [Ca2+]i response originated from podocytes. Costaining with calcein allowed the identification of podocytes because of the characteristic morphology and location in relationship to the capillary network.

Conclusions: These data suggest that podocytes in the intact glomerulus respond to Ang II with an increase of [Ca2+]i via an AT1 receptor.

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus - PubMed

......

Androgenetic alopecia in males: a histopathological and ultrastructural study.

Background Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process. Aims To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (AGA). Patients/methods Fifty-five subjects were included in this study (40 with AGA and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study. Results The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases. Conclusion Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.

Androgenetic alopecia in males: a histopathological and ultrastructural study - PubMed

..........

Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites​

Abstract​

Taurine is a non-protein sulfur aminoacid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostatis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 μmoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginin vasopressine were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340±43 to 817±116 μl/min (p<0.01); urinary sodium from 13.8±3 to 26.3±4 μmoles/min (p<0.05). Both values returned to normal after 2–3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7±2.2 to 4.3±1.9 ng/ml/hr, p<0.05) and aldosterone (from 588±47 to 348±89 pg/ml, p<0.05), but no changes in atrial natriuretic peptide and arginin vasopressine. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.

Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites

.............

Taurine prevents fructose-diet induced collagen abnormalities in rat skin​

Abstract​

Objective: The aim of the study is to investigate the effect of taurine administration on the content and characteristics of skin collagen in high-fructose-fed rats.
Research design and methods: Adult male Wistar rats were divided into four groups of six each: a control group (CON) and a taurine-supplemented control group (CON+TAU), a high fructose diet-fed group (FRU), and a taurine supplemented fructose diet-fed group (FRU+TAU). After 30 days, collagen was isolated from the skin, and its physicochemical properties were studied.
Results: Fructose administration caused an accumulation of collagen and extensive cross-linking. This was evidenced by increases in glycation, fluorescence, and peroxidation in collagen samples. The physicochemical properties of collagen, like shrinkage temperature, aldehyde content, solubility pattern, and susceptibility to denaturing agents, were altered in the fructose-fed rats. The sodium dodecyl sulphate-polyacrylamide gel electrophoretic (SDS-PAGE) pattern of collagen from fructose-fed rats showed and elevated beta component of Type I collagen. Simultaneous administration of taurine alleviated these changes.
Conclusion: The positive influence of taurine on both collagen content and its properties suggests a potential mechanism for the ability of taurine to delay diabetic complications.

...........


Effect of taurine on wound healing​

Summary​

Taurine which has antioxidant effects is also known to have effects on cell proliferation, inflammation and collagenogenesis. The aim of this study was to investigate the effect of taurine on incisional skin wounds.
The mice incised on the dorsal area were divided into control and experimental groups. Saline was injected intraperitoneally to half of the animals in the control group and locally applied to the other half. Fifty mM taurine solution was given intraperitoneally to the first half of the experimental animals and locally to the second half of the experimental group.
After four days of treatment, malondialdehyde (MDA) and histamine levels as well as the tensile strength of the wound tissue were measured. Structural alterations in epidermis and dermis were histologically evaluated.
The locally administreated taurine significantly increased wound tensile strength by decreasing the MDA and histamine levels and prevented the degranulation of the mast cells. These observations suggest that taurine may be useful on wound healing.

.........

A cell-based system for screening hair growth-promoting agents.

Androgen-inducible transforming growth factor beta (TGF-beta1) derived from dermal papilla cells (DPCs) is a catagen inducer that mediates hair growth suppression in androgenetic alopecia (AGA). In this study, a cell-based assay system was developed to monitor TGF-beta1 promoter activity and then used to evaluate the effects of activated TGF-beta1 promoter in human epidermal keratinocytes (HaCaT). To accomplish this, a pMetLuc-TGF-beta1 promoter plasmid that expresses the luciferase reporter gene in response to TGF-beta1 promoter activity was constructed. Treatment of HaCaT with dihydrotestosterone, which is known to be a primary factor of AGA, resulted in a concentration-dependent increase in TGF-beta1 promoter activity. However, treatment of HaCaT with the TGF-beta1 inhibitor, curcumin, resulted in a concentration-dependant decrease in TGF-beta1 expression. Subsequent use of this assay system to screen TGF-beta1 revealed that HaCaT that were treated with apigenin showed decreased levels of TGF-beta1 expression. In addition, treatment with apigenin also significantly increased the proliferation of both SV40T-DPCs (human DPCs) and HaCaT cells. Furthermore, apigenin stimulated the elongation of hair follicles in a rat vibrissa hair follicle organ culture. Taken together, these findings suggest that apigenin, which is known to have antioxidant, anti-inflammatory, and anti-tumor properties, stimulates hair growth through downregulation of the TGF-beta1 gene. In addition, these results suggest that this assay system could be used to quantitatively measure TGF-beta1 promoter activity in HaCaT, thereby facilitating the screening of agents promoting hair growth.

A cell-based system for screening hair growth-promoting agents - PubMed

............

Maybe a solution based on taurine, caffeine and niacin is more effective.


Taurine and niacin block lung injury and fibrosis by down-regulating bleomycin-induced activation of transcription nuclear factor-kappaB in mice​


Abstract​

The effects of taurine (T) and niacin (N) on bleomycin (BL)-induced increased production of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-6, and transforming growth factor-beta (TGF-beta) levels in the bronchoalveolar lavage fluid (BALF), and increased collagen content and nuclear factor-kappaB (NF-kappaB) activation in the lungs were investigated in mice. The mice were intratracheally instilled with saline (SA) or BL (0.1 U/mouse/50 microliter) under ketamine and xylazine anesthesia. They had ad libitum access to diet containing 2.5% niacin (w/w) or the same control diet (CD) and water with and without taurine (1%) 3 days before intratracheal instillation and throughout the study. The mice were sacrificed at different times for collecting BALF and lungs, which were appropriately processed for various measurements. Treatment with taurine and niacin attenuated the BL-induced increases in proinflammatory cytokines such as IL-1alpha, TNF-alpha, IL-6, and TGF-beta in BALF and lung hydroxyproline content of the mice in BL + TN groups. Reverse transcription-polymerase chain reaction analysis of total RNA from whole lung was performed to assess the induction of TNF-alpha and IL-1 mRNAs as markers of NF-kappaB activation. The NF-kappaB DNA-binding activity in whole-lung extract was evaluated by electrophoretic mobility shift assay. This revealed a progressive increase in NF-kappaB activation and IkBalpha depletion in lungs from mice in BL + CD groups from day 1 through day 21 compared with the corresponding SA + CD control groups. Treatment with taurine and niacin generally inhibited the BL-induced increases in the nuclear localization of NF-kappaB and preserved IkappaBalpha protein in BL + TN groups. This may be one of the mechanisms for the antifibrotic effect of taurine and niacin.

 
Last edited:

Inaut

Member
Joined
Nov 29, 2017
Messages
2,284
I think there are several ways in which taurine could help with hair loss. I haven't tested it yet, I was just curious to read about it. A possible mechanism for improving the quality of hair by taurine is inhibition of the renin angiotensin aldosterone system, regulation of intracellular calcium, prevention of excess collagen, anti-fibrotic and anti-stress (adrenal hyperactivity) and many other ways.

...

The Wnt/β-catenin pathway is known to positively affect mammalian HF growth and cycling (Andl et al., 2002; Ito et al., 2007). After activation, β-catenin accumulates in the cytoplasm and then translocates to the nucleus, where it interacts with Lef/Tcf transcription factors to regulate the expression of genes responsible for HF growth. The activity of β-catenin, the key molecule in the Wnt/β-catenin pathway, can be suppressed by glycogen synthase kinase-3β (GSK-3β), which is inhibited by phosphorylation. DHT abrogates the ability of dermal papilla cells (DPCs) from patients with AGA to induce HF stem cell differentiation via inhibition of the Wnt/β-catenin pathway in DPCs, which involves inhibiting GSK-3β activity (Mulholland et al., 2005). Therefore, we hypothesized that the Wnt/β-catenin pathway is essential to HF growth regulation by DHT.

The present study shows that the impact of DHT on HF growth and cycling varies at different concentrations by interacting with the Wnt/β-catenin signaling pathway.
We provide evidence that activation of the Wnt/β-catenin pathway can weaken the negative influence of high-dose DHT on HFs.

Dihydrotestosterone Regulates Hair Growth Through the Wnt/β-Catenin Pathway in C57BL/6 Mice and In Vitro Organ Culture

.....

Dickkopf 1 promotes regression of hair follicles​

Abstract​

Recently, we suggested that Dickkopf 1 (DKK-1) is a pathogenic mediator involved in male pattern baldness. As premature catagen onset is a key characteristic of male pattern baldness, in this study, we evaluated whether DKK-1 has a role as a catagen inducer in hair cycling. Herein, we report that recombinant human DKK-1 (rhDKK-1) injection into the hypodermis of mice during anagen caused premature onset of catagen, whereas neutralizing DKK-1 antibody delayed anagen-to-catagen transition in mice. Moreover, treatment with rhDKK-1 led to a decrease in final hair follicle length, whereas DKK-1 antibody led to an increase compared with control animals. In addition, DKK-1 and DKK-1 messenger RNA expression is most upregulated in follicular keratinocytes of late anagen in depilation-induced hair cycle progression. Moreover, we observed that rhDKK-1 blocks canonical Wnt-mediated activation of β-catenin signaling and induces the proapoptotic protein Bax, resulting in apoptosis in outer root sheath keratinocytes. Taken together, our data strongly suggest that DKK-1 is involved in anagen-to-catagen transition in the hair cycle by regulating the activity of follicular keratinocytes.

Dickkopf 1 promotes regression of hair follicles - PubMed



Oxidative stress management in the hair follicle: Could targeting NRF2 counter age-related hair disorders and beyond?​

Abstract​

Widespread expression of the transcription factor, nuclear factor (erythroid-derived 2)-like 2 (NRF2), which maintains redox homeostasis, has recently been identified in the hair follicle (HF). Small molecule activators of NRF2 may therefore be useful in the management of HF pathologies associated with redox imbalance, ranging from HF greying and HF ageing via androgenetic alopecia and alopecia areata to chemotherapy-induced hair loss. Indeed, NRF2 activation has been shown to prevent peroxide-induced hair growth inhibition. Multiple parameters can increase the levels of reactive oxygen species in the HF, for example melanogenesis, depilation-induced trauma, neurogenic and autoimmune inflammation, toxic drugs, environmental stressors such as UV irradiation, genetic defects and aging-associated mitochondrial dysfunction. In this review, the potential mechanisms whereby NRF2 activation could prove beneficial in treatment of redox-associated HF disorders are therefore discussed.

Oxidative stress management in the hair follicle: Could targeting NRF2 counter age-related hair disorders and beyond? - PubMed

….

In the present study, we found that taurine significantly increased the expression of β-catenin and that the protective effects induced by taurine are partially eliminated by a Wnt/β-catenin signaling inhibitor (i.e., DKK1). Interestingly, the inhibition of β-catenin by DKK1 not only led to elevated oxidative stress and reduced ALP but also caused the decreased expression of ERK, compared to taurine-treated cells. These results suggest that taurine inhibits oxidative stress-induced apoptosis and promotes osteoblast mineralization by activating the Wnt/β-catenin signaling pathway. More importantly, we found that Wnt/β-catenin signaling can regulate ERK phosphorylation, thereby increasing antioxidant response to oxidative stress.

Our findings indicate that taurine activates Nrf2, induces the expression of antioxidant enzymes (i.e., NQO1, HO1, and GCLC), and reduces H2O2-induced cell death by activating ERK and the Wnt/β-catenin pathway in osteoblast cells. Considering the partial reduction of ERK, antioxidants, and ALP activities by DKK1, a Wnt/β-catenin inhibitor, it is possible that other signaling molecules and pathways could be involved (Fig. 5). Thus, to explore other pathways that likely participate in taurine-mediated antioxidant effects, such as the PI3K/AKT signaling pathway (Jang et al., 2016), further research is necessary.

Cytoprotective Effect of Taurine against Hydrogen Peroxide-Induced Oxidative Stress in UMR-106 Cells through the Wnt/β-Catenin Signaling Pathway
.............

The site of taurine uptake, i.e. the hair bulb, is an area where a highly active cellular proliferation takes place, one of the most active in the whole body and from which all different follicular compartments originate [36]. This compartment is structurally and functionally surprisingly stable, since, when grown in a totally defined medium, isolated hair follicle keeps producing a normal hair fibre [18, 37]. Moreover, survival rate in vitro is increased when isolated human hair follicles are grown in the presence of taurine. These findings strongly suggest that taurine could be involved in the maintenance of human hair bulb either as an osmolyte [4, 13, 14, 38] or a regulator of cysteine and/or calcium metabolism [35].

Alternatively, it is now well established that during the development of androgenetic alopecia and the progressive transformation of terminal into vellus‐like follicles, inflammatory events occur that precede perifollicular fibrosis and ultimately sclerosis of collagenous streamers [15-17]. In this respect, taurine was described as a protective agent against age‐related progressive renal fibrosis in rats [39]. As one of the master switches of the fibrotic program is TGF‐β1, a growth factor known to inhibit hair growth in vitro [19], and since taurine can inhibit collagen synthesis [9], a down‐stream response to TGF‐β1 [40], we further investigated a possible protective role of taurine against TGF‐β1‐induced alterations. Interestingly, the most conspicuous effect of TGF‐β1 treatment was the curvature of hair follicle bulb, accompanied by a thickening of the dermal sheath as demonstrated by collagen staining. In fact, this phenomenon likely resulted from combined dermal sheath myofibroblast activation [41] and inhibition of matrix keratinocyte proliferation [19, 42, 43]. Taurine treatment dramatically counteracted this effect through a biological mechanism which remains to be explained.

Error - Cookies Turned Off

..........

Simulative evaluation of taurine against alopecia caused by stress in Caenorhabditis elegans​

Abstract​

Hair loss or alopecia has been portrayed as a modern malady which is aggravated by stressful conditions. Major cases of alopecia were found among individuals of 40s-50s, nowadays, even among the 20s-30s. This study characterized taurine's potential against alopecia caused by chemical stress agents based on the comparison with other commercially available anti-alopecia agents using Caenorhabditis elegans. The criteria used are their effects on the expression of stress markers and measurements of vital signs: lifespan comparison, progeny number, and mobility. C. elegans showed the typical stress symptoms under treatment with tunicamycin, endoplasmic reticulum stress agent. Hsp-70 protein expression increased, while worm's lifespan and per capita progeny number significantly decreased along with an unusually retarded movement. A positive response was shown when worms were treated with taurine along with astressin-B and finasteride. Between the treatments, finasteride showed better outcomes in terms of stress-reducing effects. Taurine helped worms recover more effectively from adverse influence of stress. In conclusion, there is strong evidence that taurine has a great potential as anti-alopecia effect especially against the one caused by the chemical stress. The present study implies that taurine might strongly work against hair loss when used in combination with other commercially available -anti-alopecia agents.

Simulative evaluation of taurine against alopecia caused by stress in Caenorhabditis elegans - PubMed

............

The mechanisms of taurine mediated protection against cell damage induced by hypoxia and reoxygenation

Abstract

Taurine administered during hypoxia markedly reduced the cell damage due to O2 deficiency and reoxygenation. Different mechanisms are responsible for the improved survival of the renal cell cultures. Taurine markedly reduces the osmoregulatory deterioration during hypoxia and reoxygenation. Calcium homeostasis was markedly improved. Ca2+ efflux during hypoxia as well as Ca2+ overload during reoxygenation was significantly reduced by the amino acid. The effect of taurine was partly comparable to the effect induced by Ca2+ channel blockers. One of the effects mainly responsible for cellular protection seems to be the taurine-induced acceleration of cellular growth processes in spite of hypoxia and reoxygenation. The spectrum of cytoprotective effects of taurine predisposes this substance to be a physiological protective agent responsible for cellular homeostasis or enantiostasis.

The mechanisms of taurine mediated protection against cell damage induced by hypoxia and reoxygenation - PubMed

.............

Interaction between the actions of taurine and angiotensin II

Abstract

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.

Interaction between the actions of taurine and angiotensin II - PubMed


................

Effects of Taurine on ACE, ACE2 and HSP70 Expression of Hypothalamic-Pituitary-Adrenal Axis in Stress-Induced Hypertensive Rats​

Abstract​

The experiment was to elucidate protective mechanism of taurine against stress-induced hypertension. Thirty two male Wistar rats were randomly divided into four groups. Normal control group and stress control group were intragastrically administered saline; β-alanine stress group were fed with β-alanine (200 mg/kg/day) and taurine stress group with taurine (200 mg/kg/day). The hypertensive model was established by giving rats stress for 3 weeks.Results showed that significant expression levels of angiotensin converting enzyme (ACE) in the hypothalamus, pituitary and adrenal were observed in β-alanine stress group and stress control group (P < 0.05), but significant mRNA expression levels of angiotensin-converting enzyme 2 (ACE2) in taurine stress group and normal control group (P < 0.05). All the groups showed no significant differences in HSP70 mRNA expression levels in hypothalamus (P > 0.05), while taurine stress group exhibited the highest HSP70 mRNA expression levels both in pituitary and in adrenal (P < 0.05). It was also found that β-alanine stress group and stress control group had significantly higher protein expression levels of ACE in hypothalamus, pituitary and adrenal (P < 0.05), but significantly lower protein expression of ACE2 compared to taurine stress group and control groups (P < 0.05). The results indicated that taurine regulated the hypothalamus pituitary adrenal (HPA) axis of the renin-angiotensin-aldosterone system (RAAS) by inhibiting ACE gene and protein expressions and promoting ACE2 and HSP70 protein expressions, thereby contributing to the prevention of stress-induced hypertension.

Effects of Taurine on ACE, ACE2 and HSP70 Expression of Hypothalamic-Pituitary-Adrenal Axis in Stress-Induced Hypertensive Rats - PubMed

.............

Effects of Taurine on Blood Index of Hypothalamic Pituitary Adrenal (HPA) Axis of Stress-Induced Hypertensive Rat​

Abstract​

To elucidate the protective mechanism of taurine against stress induced hypertension, 32 male Wistar rats were randomly divided into four groups: normal control group; stress control group; β–alanine stress group and taurine stress group. Rats of the two control groups were administered physiological saline while the β–alanine treated group was administered β–alanine (200 mg/kg/day) and the taurine treated group was administered taurine (200 mg/kg/day). The hypertensive model was produced by stressing the rats for 3 weeks. Serum levels of angiotensin converting enzyme (ACE), angiotensin II (AngII), glucocorticoid hormone (CRH), adrenocorticotropic hormone (ACTH), Glucocorticoid (GC), epinephrine (EPI), norepinephrine (NA) in the β–alanine stress group was significantly higher than those of the other groups (P < 0.05). However, serum of the taurine stress group contained more angiotensin converting enzyme 2 (ACE2) than those of the other groups (P < 0.05). These data indicate that taurine regulates the hypothalamus pituitary adrenal (HPA) axis of the renin-angiotensin-aldosterone system (RAAS), thereby contributing to the prevention of stress-induced hypertension.

Effects of Taurine on Blood Index of Hypothalamic Pituitary Adrenal (HPA) Axis of Stress-Induced Hypertensive Rat

..........

Effect of taurine on alteration in adrenal functions induced by stress

Abstract

When rats were exposed to immobilized cold stress, adrenaline content in the adrenal gland as well as noradrenaline content in the brain stem were reduced drastically, while noradrenaline content in the atria was not altered by the application of stress. Oral administrations of taurine (4-7 g/kg/day, for 3 days) prevented the stress-induced decline of adrenaline in the adrenal gland and this preventive effect could not be duplicated by the administration of L-isoleucine or DL-methionine. In hypophysectomized rats, the stress also induced a significant fall in adrenaline content of the adrenal gland, however taurine administration did not show significant preventive effects on the decline in adrenal catecholamines. The immobilized cold stress induced a significant increase in blood sugar and this increase was antagonized by pretreatment with taurine. Taurine had no significant effects on the stress-induced increase in the activity of adrenal tyrosine hydroxylase and the turnover rate of adrenaline in the adrenal gland measured by the rate of decline of this amine following alpha-methyl-tyrosine administration. The administration of taurine, in both in vivo and in vitro, inhibited the release of adrenaline from adrenal medullary granules, but that of dopamine-beta-hydroxylase was not significantly affected. The stress-induced elevation of the blood level of corticosterone was not affected by taurine administration. These findings indicate that taurine antagonizes the stress-induced elevation of blood sugar by reducing adrenaline output from the adrenal gland. The regulatory mechanism most likly involves the inhibition of adrenaline release from adrenal medullary granules, possibly by stabilizing the membrane of the granules.

Effect of taurine on alteration in adrenal functions induced by stress - PubMed

......

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease​

Abstract​

Taurine is a non-protein amino acid that is expressed in the majority of animal tissues. With its unique sulfonic acid makeup, taurine influences cellular functions, including osmoregulation, antioxidation, ion movement modulation, and conjugation of bile acids. Taurine exerts anti-inflammatory effects that improve diabetes and has shown benefits to the cardiovascular system, possibly by inhibition of the renin angiotensin system. The beneficial effects of taurine are reviewed.

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease - PubMed

................

Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons​

Abstract​

Glutamate-induced excitotoxicity has been implicated as an important mechanism underlying a variety of brain injuries and neurodegenerative diseases. Previously we have shown that taurine has protective effects against glutamate-induced neuronal injury in cultured neurons. Here we propose that the primary underlying mechanism of the neuroprotective function of taurine is due to its action in preventing or reducing glutamate-induced elevation of intracellular free calcium, [Ca(2+)](i). This hypothesis is supported by the following findings. First, taurine transport inhibitors, e.g., guanidinoethyl sulfonate and beta-alanine, have no effect on taurine's neuroprotective function, suggesting that taurine protects against glutamate-induced neuronal damage through its action on the extracellular membranes. Second, glutamate-induced elevation of [Ca(2+)](i) is reduced to the basal level upon addition of taurine. Third, pretreatment of cultured neurons with taurine prevents or greatly suppresses the elevation of [Ca(2+)](i) induced by glutamate. Furthermore, taurine was found to inhibit the influx but not the efflux of (45)Ca(2+) in cultured neurons. Taurine has little effect on the binding of [(3)H]glutamate to the agonist binding site and of [(3)H]MDL 105,519 to the glycine binding site of the N-methyl-D-aspartic acid receptors, suggesting that taurine inhibits (45)Ca(2+) influx through other mechanisms, including its inhibitory effect on the reverse mode of the Na(+)/Ca(2+) exchangers (Wu et al. [2000] In: Taurine 4: taurine and excitable tissues. New York: Kluwer Academic/Plenum Publishers. p 35-44) rather than serving as an antagonist to the N-methyl-D-aspartic acid receptors.

Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons - PubMed

............

Taurine increases mitochondrial buffering of calcium: role in neuroprotection

Abstract

We have determined the role of mitochondria in the sequestration of calcium after stimulation of cerebellar granule cells with glutamate. In addition we have evaluated the neuroprotective role of taurine in excitotoxic cell death. Mitochondrial inhibitors were used to determine the calcium buffering capacity of mitochondria, as well as how taurine regulates the ability of mitochondria to buffer intracellular calcium during glutamate depolarization and excitotoxicity. We report here that pre-treatment of cerebellar granule cells with taurine (1 mM, 24 h) significantly counteracted glutamate excitotoxicity. The neuroprotective role of taurine was mediated through regulation of cytoplasmic free calcium ([Ca(2+)]( i )), and intra-mitochondrial calcium homeostasis, as determined by fluo-3 and (45)Ca(2+)-uptake. Furthermore, the overall mitochondrial function was increased in the presence of taurine, as assessed by rhodamine accumulation into mitochondria and total cellular ATP levels. We specifically tested the hypothesis that taurine reduces glutamate excitotoxicity through both the enhancement of mitochondrial function and the regulation of intracellular (cytoplasmic and intra-mitochondrial) calcium homeostasis. The role of taurine in modulating mitochondrial calcium homeostasis could be of particular importance under pathological conditions that are characterized by excessive calcium overloads. Taurine may serve as an endogenous neuroprotective molecule against brain insults.

Taurine increases mitochondrial buffering of calcium: role in neuroprotection - PubMed

......

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus​

Abstract​

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus.

Background: Knowledge about biological functions of podocytes in the glomerulus is limited because of its unique anatomical location. Here we introduce a new method for measuring the intracellular calcium activity ([Ca2+]i) in the podocyte in the intact glomerulus.

Methods: With the help of fluorescence high-resolution digital imaging and a recently developed ultraviolet laser-scanning microscope, [Ca2+]i was measured in fura-2-loaded glomeruli and single podocytes of intact microdissected rat glomeruli.

Results: Angiotensin II (Ang II) increased [Ca2+]i reversibly in a biphasic and concentration-dependent manner. In contrast to Ang II, bradykinin, thrombin, arginine vasopressin, and serotonin did not change [Ca2+]i in the glomerulus. At reduced extracellular Ca2+ activity, Ang II released [Ca2+]i from intracellular stores, but the second phase, corresponding to a Ca2+ influx from the extracellular space, was absent. The L-type Ca2+ channel blocker nicardipine did not influence the Ang II-mediated [Ca2+]i increase, and an increase of the extracellular K+ concentration did not change [Ca2+]i in the glomerulus. The angrotensin II type I (AT1) receptor antagonist losartan inhibited the Ang II-mediated [Ca2+]i increase. Confocal [Ca2+]i measurements using fura-2 or fluo-3 or fluo-4 on the single cell level show that some of the Ang II-mediated [Ca2+]i response originated from podocytes. Costaining with calcein allowed the identification of podocytes because of the characteristic morphology and location in relationship to the capillary network.

Conclusions: These data suggest that podocytes in the intact glomerulus respond to Ang II with an increase of [Ca2+]i via an AT1 receptor.

Angiotensin II increases the intracellular calcium activity in podocytes of the intact glomerulus - PubMed

......

Androgenetic alopecia in males: a histopathological and ultrastructural study.

Background Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process. Aims To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (AGA). Patients/methods Fifty-five subjects were included in this study (40 with AGA and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study. Results The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases. Conclusion Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.

Androgenetic alopecia in males: a histopathological and ultrastructural study - PubMed

..........

Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites​

Abstract​

Taurine is a non-protein sulfur aminoacid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostatis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 μmoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginin vasopressine were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340±43 to 817±116 μl/min (p<0.01); urinary sodium from 13.8±3 to 26.3±4 μmoles/min (p<0.05). Both values returned to normal after 2–3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7±2.2 to 4.3±1.9 ng/ml/hr, p<0.05) and aldosterone (from 588±47 to 348±89 pg/ml, p<0.05), but no changes in atrial natriuretic peptide and arginin vasopressine. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.

Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites

.............

Taurine prevents fructose-diet induced collagen abnormalities in rat skin​

Abstract​

Objective: The aim of the study is to investigate the effect of taurine administration on the content and characteristics of skin collagen in high-fructose-fed rats.
Research design and methods: Adult male Wistar rats were divided into four groups of six each: a control group (CON) and a taurine-supplemented control group (CON+TAU), a high fructose diet-fed group (FRU), and a taurine supplemented fructose diet-fed group (FRU+TAU). After 30 days, collagen was isolated from the skin, and its physicochemical properties were studied.
Results: Fructose administration caused an accumulation of collagen and extensive cross-linking. This was evidenced by increases in glycation, fluorescence, and peroxidation in collagen samples. The physicochemical properties of collagen, like shrinkage temperature, aldehyde content, solubility pattern, and susceptibility to denaturing agents, were altered in the fructose-fed rats. The sodium dodecyl sulphate-polyacrylamide gel electrophoretic (SDS-PAGE) pattern of collagen from fructose-fed rats showed and elevated beta component of Type I collagen. Simultaneous administration of taurine alleviated these changes.
Conclusion: The positive influence of taurine on both collagen content and its properties suggests a potential mechanism for the ability of taurine to delay diabetic complications.

...........


Effect of taurine on wound healing​

Summary​

Taurine which has antioxidant effects is also known to have effects on cell proliferation, inflammation and collagenogenesis. The aim of this study was to investigate the effect of taurine on incisional skin wounds.
The mice incised on the dorsal area were divided into control and experimental groups. Saline was injected intraperitoneally to half of the animals in the control group and locally applied to the other half. Fifty mM taurine solution was given intraperitoneally to the first half of the experimental animals and locally to the second half of the experimental group.
After four days of treatment, malondialdehyde (MDA) and histamine levels as well as the tensile strength of the wound tissue were measured. Structural alterations in epidermis and dermis were histologically evaluated.
The locally administreated taurine significantly increased wound tensile strength by decreasing the MDA and histamine levels and prevented the degranulation of the mast cells. These observations suggest that taurine may be useful on wound healing.

.........

A cell-based system for screening hair growth-promoting agents.

Androgen-inducible transforming growth factor beta (TGF-beta1) derived from dermal papilla cells (DPCs) is a catagen inducer that mediates hair growth suppression in androgenetic alopecia (AGA). In this study, a cell-based assay system was developed to monitor TGF-beta1 promoter activity and then used to evaluate the effects of activated TGF-beta1 promoter in human epidermal keratinocytes (HaCaT). To accomplish this, a pMetLuc-TGF-beta1 promoter plasmid that expresses the luciferase reporter gene in response to TGF-beta1 promoter activity was constructed. Treatment of HaCaT with dihydrotestosterone, which is known to be a primary factor of AGA, resulted in a concentration-dependent increase in TGF-beta1 promoter activity. However, treatment of HaCaT with the TGF-beta1 inhibitor, curcumin, resulted in a concentration-dependant decrease in TGF-beta1 expression. Subsequent use of this assay system to screen TGF-beta1 revealed that HaCaT that were treated with apigenin showed decreased levels of TGF-beta1 expression. In addition, treatment with apigenin also significantly increased the proliferation of both SV40T-DPCs (human DPCs) and HaCaT cells. Furthermore, apigenin stimulated the elongation of hair follicles in a rat vibrissa hair follicle organ culture. Taken together, these findings suggest that apigenin, which is known to have antioxidant, anti-inflammatory, and anti-tumor properties, stimulates hair growth through downregulation of the TGF-beta1 gene. In addition, these results suggest that this assay system could be used to quantitatively measure TGF-beta1 promoter activity in HaCaT, thereby facilitating the screening of agents promoting hair growth.

A cell-based system for screening hair growth-promoting agents - PubMed

............

Maybe a solution based on taurine, caffeine and niacin is more effective.


Taurine and niacin block lung injury and fibrosis by down-regulating bleomycin-induced activation of transcription nuclear factor-kappaB in mice​


Abstract​

The effects of taurine (T) and niacin (N) on bleomycin (BL)-induced increased production of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-6, and transforming growth factor-beta (TGF-beta) levels in the bronchoalveolar lavage fluid (BALF), and increased collagen content and nuclear factor-kappaB (NF-kappaB) activation in the lungs were investigated in mice. The mice were intratracheally instilled with saline (SA) or BL (0.1 U/mouse/50 microliter) under ketamine and xylazine anesthesia. They had ad libitum access to diet containing 2.5% niacin (w/w) or the same control diet (CD) and water with and without taurine (1%) 3 days before intratracheal instillation and throughout the study. The mice were sacrificed at different times for collecting BALF and lungs, which were appropriately processed for various measurements. Treatment with taurine and niacin attenuated the BL-induced increases in proinflammatory cytokines such as IL-1alpha, TNF-alpha, IL-6, and TGF-beta in BALF and lung hydroxyproline content of the mice in BL + TN groups. Reverse transcription-polymerase chain reaction analysis of total RNA from whole lung was performed to assess the induction of TNF-alpha and IL-1 mRNAs as markers of NF-kappaB activation. The NF-kappaB DNA-binding activity in whole-lung extract was evaluated by electrophoretic mobility shift assay. This revealed a progressive increase in NF-kappaB activation and IkBalpha depletion in lungs from mice in BL + CD groups from day 1 through day 21 compared with the corresponding SA + CD control groups. Treatment with taurine and niacin generally inhibited the BL-induced increases in the nuclear localization of NF-kappaB and preserved IkappaBalpha protein in BL + TN groups. This may be one of the mechanisms for the antifibrotic effect of taurine and niacin.

Excellent post. Thanks for sharing.
 

Charger

Member
Joined
Nov 25, 2019
Messages
252
Location
Chesapeake, VA
I've been using caffeine, l-threonate, and taurine topically with stemoxydine and have noticed improved quality and thickness. Can't speak to regrowth yet.
 

Archon

Member
Joined
Dec 8, 2020
Messages
16
how do you prepare a caffeine and taurine solution? Just water? What concentration for caffeine?
I've been using caffeine, l-threonate, and taurine topically with stemoxydine and have noticed improved quality and thickness. Can't speak to regrowth yet.
 
Similar threads
Thread starter Title Forum Replies Date
D Taurine Topical Supplements, Pharmaceutical Drugs 6
milk_lover Topical Taurine Is Protective Against UV Radiation? Taurine 1
M Will topical zinc cause grey hair ? Hair & Nails 1
A Topical Gonadin/ Kuinone Diet 2
F Did anyone reversed grey hairs with topical copper? Hair & Nails 10
F Topical Tocovit Danny Roddy 9
ImprovingDaily Anyone know how to make topical Cascara Sagrada? Skin 0
M ADEK - Why are people taking it topical? Diet 3
U How much DMSO for topical solution? Supplements, Pharmaceutical Drugs 3
Pina Topical Lung T3 Treatment COVID-19 Acute Respiratory Distress Syndrome Thyroid and Hormones 0
R Safety of topical antibiotic clindamycin 1% with benzoyl peroxide 2.5% for acne? Ask For Help or Advice 0
youngsinatra Post Your Experience With Topical Vitamin A Here Metabolism 18
haidut Topical DHT therapy promotes hair growth Scientific Studies 15
M How much of topical zinc (scalp) will go systemically? Ask For Help or Advice 7
M Topical Dutasteride = no systemic absorbtion?? Hair & Nails 61
S Question about topical delivery mechanisms for scalp Hair & Nails 0
Inaut Topical Agmatine For Hair Loss Hair & Nails 3
R DMSO vs ethanol for maximum topical absorption? Ask For Help or Advice 1
G Topical DHEA for hair loss?!? Hair & Nails 46
B DHEA Solution for topical application, how to make it? Skin 11
R Topical magnesium citrate? Hair & Nails 2
A Help Stretch Marks/slight Loose Skin (oral/topical Skin 20
J Progest E Topical Ask For Help or Advice 0
GuiCHE DIY Topical Progesterone? Supplements, Pharmaceutical Drugs 2
johnwester130 Best Topical Antifungal? Hair & Nails 56
AnaU Topical Vitamin E -> Rash? Supplements, Pharmaceutical Drugs 2
E How Bad Is Topical Ciprofloxacin (Ear Drops)? Ask For Help or Advice 14
Gohan Topical Steroids Ask For Help or Advice 13
L New Topical Finasteride Hair & Nails 6
vulture Best Solvent For Topical DHEA In Genitals Thyroid and Hormones 13
L Help With Topical T3 Daily Dosage Metabolism 3
Highserotonin90 Topical Vitamins Application Experiments 0
haidut Topical DHEA Has Potent Anti-aging Effects On Human Skin Scientific Studies 8
haidut Topical T3 Dramatically Stimulates Hair Growth Scientific Studies 13
L Topical T3 For Hair Growth Hair & Nails 47
ecstatichamster Apply Topical Supplements To Your Belly Button Supplements 29
C Questions On DIY Topical B Vitamins Supplements, Pharmaceutical Drugs 51
ecstatichamster Topical Agmatine Aqueous Lowering Intraocular Pressure Eyes, Ears, Nose and Headaches/Migraines 5
wealthofwisdom Is Now Topical Progesterone Good? Ask For Help or Advice 31
L Please Help, Homemade Topical Hair Cream Hair & Nails 16
K Are You Aware Peat Does Not Believe Topical Thyroid Hormones To Be Helpful? Email Advice 21
I Topical Retinoids - Do They Really Increase Collagen Production? Skin 7
Peatogenic Topical Antifungal Options (D3 As Anti Staph?) Skin 32
Peatogenic Does Location And Variety Of Topical Application Points Affect Absorption? Supplements, Pharmaceutical Drugs 3
Ficini Niacinamide Topical Vs Oral Clarification B3/Niacinamide 2
J Topical Propecia/Finasteride For Hair Loss Hair & Nails 31
opethfeldt Progesterone Oral Vs Topical Progesterone 26
R Topical Retinoids, Good For Anything ? Supplements, Pharmaceutical Drugs 5
R Need An Opinion Regards Vitamin A Topical / Oral Supplements, Pharmaceutical Drugs 10
methylenewhite Topical Serotonin Antagonist Ketanserin Improves Wound Healing Up To 150% Scientific Studies 0

Similar threads

Top