Plants And Insects As A Source Of Steroids

[vulture]

Ecdysterone yes or no? - AnabolicMinds.com

Amen, and something I've been saying for years. In fact, the former Soviet literature concerning Rhaponticum Carthamoides speaks to a very specific grouping of ecdysteroids, referred to as the "levseins" complex. There are also tannins and resins present in this source genus, one of which mitigates carbs being stored as fat.

I've used more 20-H than I care to admit. Orally, it's a complete bust. Transdermally you'll see some of the classic Ecdy benefits (greatly mitigated DOMS, etc), but even those effects took over a gram delivered transdermally/day in a DMSO base. Ironically, it was PA's "odorless" DMSO...

Great stuff btw PA. Wish you still offered it...

I have searched and reviews seem rather confusing: there's nothing even close to concensus about Ecdysterone.

 

[LeeLemonoil]

Ursoli acid from appple peels, rosemary and others a well a especially Tomatadine seem to be powerful steroid-molecules of plant origin, structurally they are very close to androgens.

The anabolic effect of tomatidine versus that of ursolic acid
You should be able to buy it soon: tomatidine, the anabolic in tomatoes
Tomatidine, a medicine against atherosclerosis from tomatoes
Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway. - PubMed - NCBI
Keeping older muscles strong - Nutrition and Healing

 

[LeeLemonoil]

Alpha-cedrene, a completely new kind of anabolic from cedar oil

Constituent of virginian Cedar oil anabolic and ergogenic, prevents muscle and strength decline due to free fatty acids.

 

[RisingSun]

Ecdysone is the moulting hormone of arthropods.
In Drosophila melanogaster, an increase in ecdysone concentration induces the expression of genes encoding proteins that are required by the larva, and causes the formation of puff chromosomes (high expression sites). Ecdysteroids also appear in many plants, mostly as a protective agent (toxins or anti-nutrients) against herbivorous insects.
Some of the medicinal plants that include phytoecdisteroids are: Achyranthes bidentata, Tinospora cordifolia, Pfaffia paniculata, Leuzea carthamoides, Rhaponticum uniflorum, and Serratula coronata
These plants work well as adaptogens
Ecdysone closely resembles testosterone.
Will it be possible to consume the plants or insects themselves as a source of steroids ???View attachment 6884

And this is going to be significant because...?

Anything you ingest / inject that is directly a steroid or a form of steroid is going to shut down by as much as your body senses is brought from outside.

So unless you take exogenously more than your body naturally produces, the exogenous steroid route is moot at best, and dubious in the specific case of bioavalability of insect derived steroids.

 

[LeeLemonoil]

This study suggests Ecdysone acts similar to Aldosterone in humans.
Effect of β‑ecdysterone on glucocorticoid‑induced apoptosis and autophagy in osteoblasts. - PubMed - NCBI
Ecdysone Elicits Chronic Renal Impairment via Mineralocorticoid-Like Pathogenic Activities.
Lu M1,2,3, Wang P1, Zhou S1,3, Flickinger B2,4, Malhotra D2, Ge Y2,3, Tatar M5, Dworkin L2, Liu Z1, Gong R1,2,3.
Author information
Abstract
BACKGROUND/AIMS:
Ecdysteroids are steroidal insect molting hormones that also exist in herbs. Ecdysteroid-containing adaptogens have been popularly used to improve well-being and by bodybuilders for muscle growth. However, the use of ecdysone in mammals is also associated with kidney growth and enlargement, indications of disturbed kidney homeostasis. The underlying pathogenic mechanism remains to be clarified.

METHODS:
Virtual screening tools were employed to identify compounds that are homologous to ecdysone and to predict putative ecdysone-interacting proteins. The kidney effect of ecdysone was examined in vitro and in vivo and compared with that of aldosterone. Cellular apoptosis was estimated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Cell motility was assessed by scratch-wound cell migration assay. Blood urea nitrogen was measured to evaluate renal function. Western immunblot analysis was employed to determine the expression profile of interested proteins.

RESULTS:
Computational molecular structure analysis revealed that ecdysone is highly homologous to aldosterone. Moreover, virtual screening based on compound-protein interaction profiles identified the Mineralocorticoid Receptor (MR) to potentially interact with ecdysone. Accordingly, to assess potential biological functions of ecdysone in mammals, ecdysone was applied to mineralocorticoid-sensitive inner medullar collecting duct cells. Ecdysone induced mesenchymal accumulation of extracellular matrix and epithelial dedifferentiation characterized by de novo expression of α-smooth muscle actin. In addition, ecdysone elicited cellular apoptosis and retarded cell motility, akin to the effect of aldosterone. In vivo, daily treatment of mice with ecdysone increased cell apoptosis in the kidney, impaired renal function and elicited early signs of renal fibrogenesis, marked by deposition of collagen and fibronectin in tubulointerstitium, reminiscent of the action of aldosterone. The MR signaling pathway is likely responsible for the cellular and pathobiological effects of ecdysone, as evidenced by strong ecdysone-induced MR nuclear translocation in renal tubular cells both in vitro and in vivo, while blockade of MR by concomitant spironolactone treatment largely abolished the detrimental effects of ecdysone.

CONCLUSION:
Our findings suggest that ecdysone induces mineralocorticoid-dependent activities that impair renal function and elicit renal injury.


while these two suggsts ne more time it actually is a protective substance, especilally against cortisol-induced damages

Effect of β‑ecdysterone on glucocorticoid‑induced apoptosis and autophagy in osteoblasts.
Tang YH1, Yue ZS1, Li GS2, Zeng LR1, Xin DW1, Hu ZQ1, Xu CD1.
Author information
Abstract
The aim of the present study was to investigate the effect of glucocorticoids in osteoblasts and to examine the role of β‑ecdysterone in the pathogenesis of glucocorticoid‑induced osteoporosis. Osteoblasts were induced from bone marrow mesenchymal stem cells, which were isolated from C57BL/6 mice. Cell viability and apoptosis of osteoblasts were measured by Cell Counting Kit‑8 and flow cytometry analysis, respectively. The expression of related genes and proteins was measured by reverse transcription quantitative polymerase chain reaction and western blot analysis respectively. Dose‑dependent decreases in the cell proliferation and differentiation were observed in dexamethasone (Dex)‑treated osteoblasts, evidenced by downregulation in the activity of alkaline phosphatasedecreased expression levels of Runt‑related transcription factor 2 and osteocalcin, and upregulated expression of RANK ligand. Dex also induced apoptosis and inhibited autophagy of osteoblasts, evidenced by upregulated B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio and the activation of mammalian target of rapamycin (mTOR), and decreased expression levels of Beclin‑1, autophagy protein 5 and microtubule‑associated protein 1 light chain 3 II. The effects on cell proliferation, apoptosis and autophagy induced by Dex were reversed by β‑ecdysterone in a dose‑dependent manner. Therefore, β‑ecdysterone may be a promising candidate drug for the treatment of osteoporosis through inducing osteoblast autophagic activity by inactivating mTOR.

β‑Ecdysterone promotes autophagy and inhibits apoptosis in osteoporotic rats.
Tang YH1, Yue ZS1, Xin DW1, Zeng LR1, Xiong ZF1, Hu ZQ1, Xu CD1.
Author information
Abstract
Osteoporosis is an aging process of skeletal tissues with characteristics of reductions in bone mass and microarchitectural deterioration of bone tissue. The present study aimed to investigate the effects of glucocorticoid‑induced osteoporosis on osteoblasts and to examine the roles of β‑ecdysterone (β‑Ecd) involved. In the present study, an in vivo model of osteoporosis was established through the subcutaneous implantation of prednisolone (PRED) into Sprague‑Dawley rats, with or without a subcutaneous injection of β‑Ecd (5 or 10 mg/kg body weight). Expression of Beclin‑1 and microtubule‑associated protein 1A/1B‑light chain 3I/II and apoptosis in lumbar vertebrae tissues was measured by immunofluorescence and TUNEL assays, respectively. Serum concentration of calcium and phosphorus, and the activity of tartrate‑resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) were measured by biochemical assay. Reverse transcription‑quantitative polymerase chain reaction and western blotting was used for detect the expression of related genes and proteins. PRED treatment inhibited bone formation by decreasing bone mineral density, and suppressing the expression of Runt‑related transcription factor 2 and bone morphogenetic protein 2, while enhancing the activity of alkaline phosphatase, upregulating the expression of receptor activator of nuclear factor-κB ligand, and increasing the serum content of calcium, phosphorus and tartrate‑resistant acid phosphatase in rats. Additionally, PRED was revealed to inhibit autophagy through the downregulation of Beclin‑1, autophagy protein 5 and microtubule‑associated protein 1A/1B‑light chain 3I/II expression, whereas it induced the apoptosis, through the activation of caspase‑3 and the suppression of apoptosis regulator BCL2 expression. Notably, the PRED‑induced alterations in bone formation, autophagy and apoptosis were revealed to be attenuated by β‑Ecd administration. In conclusion, the findings of the present study suggested that β‑Ecd may be a promising candidate for the development of therapeutic strategies for the treatment of osteoporosis, through the induction of autophagy and the inhibition of apoptosis in vivo.

 

[LeeLemonoil]

Really hard to grasp for me, and exogenous insect and plant-hormone that acts on human mineral and Estrogen beta- Receptors and has so much promising but also cautioning research results to show for

 

[LeeLemonoil]

Anybody an idea why a steroidal substance that obviusly attenuates corticosteroid-induced catabolica nd tissue destrcuctive effects might also act as an aldosterone-homolouge?

 

[LeeLemonoil]

Ecdysterone also increases AcChE.

Ecdysterone induces acetylcholinesterase in mammalian brain.
Catalan RE, Aragones MD, Godoy JE, Martinez AM.
Abstract
The effects of ecdysterone on brain acetylcholinesterase (AChE) in immature and adult rats of both sexes have been studied in in vitro conditions. Ecdysterone produced an increase of AChE in rat brain slices. The most remarkable effect was found in immature male rats. In vitro assay using a purified AChE from electric eel showed no effect. Pretreatment with cycloheximide or actinomycin D abolished the ecdysterone action on brain AChE. These results support the idea that induction of AChE may be involved in the heterophilic action of ecdysterone.

 

[LeeLemonoil]

Two more recent publications hinting at positive effects from ß-Ecdy:


β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration.

β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration. - PubMed - NCBI

Abstract
Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β‑ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β‑ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of β‑ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that β‑ecdysterone attenuated the apoptosis induced by tert‑butyl hydroperoxide via promoting autophagy in nucleus pulposus cells. Beclin‑1, an indispensable protein for the stimulation of autophagy, is upregulated and stabilized by β‑ecdysterone in a dose‑ and time‑dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3‑methyladenine partially abrogated the protective function of β‑ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β‑ecdysterone on IDD. Additionally, β‑ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β‑ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β‑ecdysterone may be a potential therapeutic agent for IDD.


Steroid-Enriched Fraction of Achyranthes bidentata Protects Amyloid β Peptide 1-40-Induced Cognitive Dysfunction and Neuroinflammation in Rats.

Steroid-Enriched Fraction of Achyranthes bidentata Protects Amyloid β Peptide 1-40-Induced Cognitive Dysfunction and Neuroinflammation in Rats. - PubMed - NCBI

Abstract
The roots of Achyranthes bidentata Blume (AB) is commonly used in the treatment of osteoporosis and dementia in traditional Chinese medicine. Pharmacological reports evidenced that AB possessed anti-osteoarthritis effects. However, there is little literature about the anti-dementia activities of AB. The present study was designed to prepare steroid-enriched fraction of AB (ABS) and investigate whether ABS can protect from cognitive dysfunction and neuroinflammation against Aβ 1-40-induced Alzheimer's disease (AD) model in rats. ABS only contained 135.11 ± 4.28 mg of ecdysterone per gram. ABS (50 mg/kg) reversed the dysfunction of exploratory activity and memory function on plus-maze and Morris water maze caused by Aβ 1-40 in rats. ABS (50 mg/kg) also decreased amyloid deposition, neurofibrillary tangle, neural damage, activated astrocyte, and microglial caused by Aβ 1-40. Furthermore, ABS reversed the phenomenon of neural oxidative damage and neuroinflammation, including the higher levels of MDA and cytokines, and the lower activities of antioxidant enzymes and GSH levels caused by Aβ 1-40 in rat cortex and hippocampus. Finally, ABS restored the activation of ERK pathway and decreased NF-κB phosphorylation and translocation altered by Aβ 1-40. ABS alone (50 mg/kg) promoted cognitive function, activated brain antioxidant defense system, and decreased brain TNF-α levels in sham group. Therefore, ABS has the cognition-promoting and antidementia potential. Steroids especial ecdysterone are major active components of AB. The action mechanism is due to decreasing oxidative stress and neuroinflammation through modulating ERK pathway, NF-κB phosphorylation, and translocation in Aβ 1-40-induced AD rat model.

 

[LeeLemonoil]

https://www.sciencedirect.com/science/ar...4048?via%3Dihub

Phytoecdysteroid-enriched quinoa seed leachate enhances healthspan and mitochondrial metabolism in Caenorhabditis elegans


Highlights
•Quinoa enhanced C. elegans median lifespan, locomotory vigor, and mitochondrial respiration.
•Quinoa reduced AGE pigment, reactive oxygen species, and fat accumulation in C. elegans.
•20-hydroxyecdysone is a primary bioactive constituent of quinoa.

Abstract

Quinoa (Chenopodium quinoa Willd.) phytochemicals have exhibited metabolic benefit in mammals, though their effects on aging and mechanisms of action remain unknown. Caenorhabditis elegans offers a practical in vivo model to study bioactivity since major metabolic pathways are conserved across phyla. We explored the effects of phytoecdysteroid-enriched quinoa seed preparation, termed quinoa leachate (QL), on behavioral and biochemical endpoints of wild-type C. elegans health. QL treatment (1.0 mg/mL or less) increased median lifespan from 9 to 11 d, improved locomotory performance from 103.5 to 114.9 head thrashes/min, and enhanced basal respiration rate by 37%. QL also reduced advanced glycation end-product (AGE) pigments by 24%, reactive oxygen species (ROS) by 20%, and body fat by 14%. 20-Hydroxyecdysone (20HE), the primary phytoecdysteroid in QL, conferred statistically similar benefit compared to QL at equivalent doses. Data suggest that quinoa supplementation slows C. elegans aging and improves metabolic health, and 20HE is the primary bioactive constituent responsible for favorable effects.

Bedanken

 

[Sativa]

Don't forget this aspect -
Ecdysteroids may be a form of, or have a similar role to vitamin D...

according to this well-reputed insect-researcher:
Are Ecdysteroids insect hormones? – Atlas of Science
I have linked up a lot of publications here on RP-Forum that show a lot of beneficial effects of Ecdysteroids,
virtually every peaty-parameter seem to be modulated in a positive way.

Plants And Insects As A Source Of Steroids
There are reservations because some ecdysteroids bind to ERbeta but that does not concern me - on the contrary given that interesting steroids like the Androstanediols, DHEA and substances Tocotrienols bind them too and displace E2 and excert protective effects this way.

Others are skeptical because of the molting hormone/prolactin Connection but this author has rather convincingly explained that ecdysteroids are not insect-hormones nor are they really the initiator of molting.

And lastly, a recent publication in Nature claims a structural and activity relationship between ecdysterone and aldosterone (which really would be a cause for caution), but that seems to be true only for alpha-Ecdysone which is the non-hydroxylated form and is likely of no importance in vivo.

What do you make of the thesis that ecdysteroids might be essential Vitamin-D sterols in humans? I find it highly intriguing and especially the hydroxylation and glycoside structures hint at the possibility. The "peat"- Flavones like Apigenin are now also considered hormone-like especially their glycsosides.

 

[LeeLemonoil]

Thanks @Sativa, didn’t forget my own postings.

Slama has debunked the wrong assumption that Ecdysterone are insect-hormones, neither are they molting hormones therefore.
We can forgetabout the prolactin connection thus, Peat was wrong on that, but he claimed that decades ago, Slamas research is very new.

 

[LeeLemonoil]

ß-Ecdysterone gets pharma attention. How practical that recently there was a push to ban it as a supp becuase it is "doping"

https://www.researchgate.net/public...the_renin_angiotensin_system_via_Mas_receptor

20-Hydroxyecdysone (20E) is a steroid hormone that plays a key role in insect development through nuclear ecdysone receptors (EcRs) and at least one membrane GPCR receptor (DopEcR) and displays numerous pharmacological effects in mammals. However, its mechanism of action is still debated, involving either an unidentified GPCR or the estrogen ER receptor. The goal of our study was to better understand 20E mechanism of action. A mouse myoblast cell line (C2C12) and the gene expression of myostatin (a negative regulator of muscle growth) was used as a reporter system of anabolic activity. Experiments using protein-bound 20E established the involvement of a membrane receptor. 20E-like effects were also observed with Angiotensin-(1-7), the endogenous ligand of Mas. Additionally, the effect on myostatin gene expression was abolished by Mas receptor knock-down using small interfering RNA (siRNA) or pharmacological inhibitors. 17-Estradiol (E2) also inhibited myostatin gene expression, but protein-bound E2 was inactive, and E2 activity was not abolished by angiotensin-(1-7) antagonists. A mechanism involving cooperation between Mas receptor and a membrane-bound palmitoylated estrogen receptor is proposed.The possibility to activate the Mas receptor with a safe steroid molecule is consistent with the pleiotropic pharmacological effects of ecdysteroids in mammals and indeed this mechanism may explain the close similarity between angiotensin-(1-7) and 20E effects. Our findings open a lot of possible therapeutic developments by stimulating the protective arm of the renin-angiotensin-aldosterone system (RAAS) with 20E.

 

[LeeLemonoil]

a new study substantiating the very pro-metabolic effects of Ecdy that were often reported in older studies

20-Hydroxyecdysone Ameliorates Metabolic and Cardiovascular Dysfunction in High-Fat-High-Fructose-Fed Ovariectomized Rats - PubMed

Background: Ecdysteroids are polyhydroxylated steroids present in invertebrates and plants. 20-Hydroxyecdysone (20E) is the most common and the main biologically active compound of ecdysteroids. Previous studies have demonstrated anabolic and metabolic effects of 20E in mammals. However, it is unknown whether 20E has a positive effect on all aspects of cardiometabolic syndrome. The aims of this study were to investigate the favorable effect and possible underlying mechanisms of 20E in a rat model of cardiometabolic syndrome (CMS) induced by a high-calorie diet combined with female sex hormone deprivation.

Methods: 20E (5 mg/kg, 10 mg/kg, or 20 mg/kg) or pioglitazone (PIO) (10 mg/kg) was intragastrically administered to sham-operated Sprague-Dawley female rats and ovariectomized rats fed a high-fat-high-fructose diet (OHFFD) for 8 weeks. The phenotypic characteristics of CMS, including central adiposity, blood pressure, serum lipid profile, glucose tolerance, insulin action on skeletal muscle glucose transport activity and hepatic protein expression, were determined.

Results: Some CMS characteristics were improved by 20E treatment. Rats treated with 20E had lower body weight, abdominal fat accumulation than rats treated with vehicle control without changes in total caloric intake and fat-free mass. OHFFD rats exhibited high blood pressure, but 20E-treated rats maintained normal blood pressure with a lower level of low-density lipoprotein (LDL)-cholesterol. Although 20E showed no positive effect on inducing insulin-mediated glucose transport in the skeletal muscle of OHFFD rats, 20E improved whole body glucose homeostasis. Analysis of protein expression in livers from 20E-treated rats revealed significantly increased expression of pAkt Ser473, pFOXO1 Ser256, pAMPKα Thr172, and FGF21.

Conclusion: 20E treatment can alleviate cardiometabolic disorder caused by a high-fat-high-fructose diet and female sex hormone deprivation. In particular, 20E helps improve whole body insulin sensitivity in OHFFD rats, and the mechanisms that underlie this favorable effect are potentially mediated by the activation of AMPK and FGF21. The present study indicates that 20E could be an alternative therapeutic option for the prevention and alleviation of cardiometabolic syndrome.

@Amazoniac

 

[LeeLemonoil]

Ecdysterone kills breast cancer cells


Women who consume a relatively large amount of ecdysterone through supplements or foods like spinach and quinoa may protect themselves against breast cancer. And for women who already have breast cancer, ecdysterone may make chemo treatments more effective. Molecular biologists from the Russian Academy of Sciences in Petersburg come to this conclusion in Frontiers in Pharmacology.



Study
The researchers exposed cancer cells in Petri dishes to ecdysterone. The Russians experimented with hormone-sensitive MCF-7 breast cancer cells and with two hormone-insensitive breast cancer cell types, MDA-MB-468 and MDA-MD-231. Below we limit ourselves to the results of the tests with MCF-7 cells. The results of the experiments with the other cell types were not essentially different.

Results
When the researchers exposed healthy cells to the same concentrations, they were found to be resistant to ecdysterone. Cancer cells responded differently. Ecydysterone killed the breast cancer cells, you can see below. The lower the absorbance in the figure below, the lower the viability of the cells.

The dots above are colonies of breast cancer cells. Since ecdysterone decreases the formation of colonies, you might hypothesize that ecdysterone may be able to slow the spread of breast cancer cells.



Even better were the results of experiments in which the Russians simultaneously exposed breast cancer to both ecdysterone and the cytostatic doxorubicin, a substance that oncologists administer in chemotherapy. Ecdysterone made doxorubicin even more deadly to the cancer cells.

Mechanism


Ecdysterone disrupts the energy balance of breast cancer cells, the Russians discovered. This makes the cells more vulnerable.


Incidentally, ecdysterone also enhanced the effect of exposure with the glucose analogue 2-deoxy-glucose. Cells cannot convert 2-deoxy-glucose into energy, but the analog can displace glucose. To a certain extent, we speculate cheerfully and without too much knowledge, administration of 2-deoxy-glucose imitates the effects of a low-carbohydrate diet.



Conclusion
"Our results indicate that ecdysterone can be considered as a new potential adjuvant for genotoxic therapy in treatment of breast cancer patients", write the researchers. "Furthermore, since ecdysterone enhances the ability to cope with stress and enhances resistance to tiredness, it seems beneficial to administer it as part of cytotoxic therapy with doxorubicin."



"However, additional experiments aimed at the elucidation of effectiveness of ecdysterone and its toxicity to organs and tissues are required to assess the therapeutic potential of ecdysterone as an adjuvant therapy to treat breast cancer."

 

[Brandin]

And this is going to be significant because...?

Anything you ingest / inject that is directly a steroid or a form of steroid is going to shut down by as much as your body senses is brought from outside.

So unless you take exogenously more than your body naturally produces, the exogenous steroid route is moot at best, and dubious in the specific case of bioavalability of insect derived steroids.

Not if your genetical homeostasis and expressions of hormones is different than the state u are in.