Peatish Eyedrops

[LeeLemonoil]

These eyedrops with Vit B2 promote B2 as an active that „absorbs“ or protects against UV and bluelight and is recommended for monitor work. Can’t vouch for the legitimacy of such claims.

Augentropfen spezielles UV-Licht

Barriere zum Schutz vor blauem Licht durch Geräte und UV-Strahlung

de.farmaciacastellanos.com

 

[LeeLemonoil]

Im still interested in methylene blue for eye and specifically corneal health.

Since MB can influence cell metabolism positively and also shows good effects in remodulating Extraellular Matrix more healthily by readjusting MMP balance it seems very useful potentially for Keratoconus.
There are existing eyedrops with it as shown in this thread.

Some tricky questions remain though:

Skincells anti-aging effects were best at concentrations of 0.5-2.5 micromol. That’s a tiny dose. But in cell cultures, will that work in real life use / eyedrops? Or would concentration needed to be upped?

Also. Blue. We know the metabolic benefits of red to orange spectrums and blue spectrums need to be treated cautiously for cell metabolism.

What Would MB in eyedrops do? Eben at doses that Are hardly blue? Will they prevent red spectras from entering the eye and being net negative?

Or does MB deflect blue lights maybe and this having another benefit?

@haidut
Would you mind looking at this post and the one below

 

[LeeLemonoil]

Also in this publication on Quercetin as a treatment agent for various eye issues the section on Keratoconus outlines the metabolic effects and the efficacy of metabolic modulation in Keratoconus.

Quercetin is hardly water soluble and has other issues which makes it a poor choice for eyedrop use.
Can you think of other water soluble, tolerable substances that could bring metabolic benefits in corneal cells when used in low concentrations topicals?
(Taurine at 2% works fine btw, doesn’t sting either)


Quercetin:

1. Keratoconus​

Keratoconus is an ocular disease that seriously impairs vision. In patients with keratoconus, the corneal extracellular matrix is obviously lost, lactate is significantly elevated, and the cornea gradually thins and protrudes forward. In advanced stages, patients deteriorate with acute corneal edema, corneal scarring, severe vision loss, and eventually require corneal transplantation treatment [37], [38], [39]. Currently, there is no method to reverse or restore the loss of extracellular matrix and produce a more normal stromal-like cornea.

The antioxidant and anti-fibrotic activities of quercetin make it possible to reduce scarring in keratoconus and other fibrosis-related diseases. Any disruption of collagen mechanical properties, collagen structure, and collagen-ligase activity in patients with keratoconus may result in altered extracellular matrix assembly and defective corneal structures. In addition, the changes in key energy metabolic pathways can lead to a large accumulation of lactate in cells [13], [40]. As reported, lactate is a metabolite that is highly regulated in both human keratoconus cells and keratoconus corneal buttons. It causes corneal edema and promotes fibrosis during wound healing by activating the transforming growth factor-β (TGF-β) signaling pathway. McKay et al. [13] found that quercetin could downregulate the expression of TGF-βRII and TGF-β2 in human keratoconus cells through the TGF-β signaling pathway, significantly reduce the secretion of type III
collagen in the extracellular matrix and the expression of pro-fibrosis molecules, and further inhibit corneal fibrosis. In another study, McKay and coworkers found that quercetin directly regulates the expression of glycolytic enzymes and increases glucose-6-phosphate, which increases the glycolytic metabolites and metabolite flux in the pentose phosphate pathway, reduces the secretion of lactate in keratoconus stromal cells, and promotes ATP production in the citric acid cycle to restore the balance of ATP-ADP-AMP in human keratoconus cells [40]. Therefore, quercetin is a strong antioxidant that can inhibit corneal fibrosis by inhibiting scar formation and modulating cellular metabolism. At the same time, quercetin is also an effective inhibitor of fibrosis markers in keratoconus and is a key regulator of extracellular matrix assembly.

The therapeutic use of quercetin in ophthalmology: recent applications

Quercetin is a natural flavonol antioxidant found in various plant sources and food samples. It is well known for its notable curative effects on the …

www.sciencedirect.com

 

[LeeLemonoil]

B2 solution dropped onto the cornea and then radiate it with UV-light is currently on of the „State of the Art“ trestmevg for Keratoconus. It often halts the further Progression of the disease and stiffens and flattens the konic cornea

But no one in mainstream ever explained why and what’s the mechanism.

Some outsiders speculate pathogens to be the cause of KC, Mainstream Sais it’s aseptic inflammation / autoimmume.

Well B2 seems to be able to work on many Keratoconus related fronts: increasing metabolism. Bring antibiotic. Bring anti LPS. And also as this post shows some special keratocyte related actions.

My hunch is that, along with diet changes, early diagnosed KC could be helped greatly with some simpler eye drop ingredients but no one wants to research that.

This is just a follow up on the recent post on both riboflavin and vitamin D.
Vitamin B2 Remarkably Effective Against Endotoxin, Sepsis, And Other Bacterial Infections
Vitamin D Is Endotoxin (LPS / TLR4) Antagonist, May Treat LPS-linked Conditions

Endotoxin (TLR4) antagonists are very beneficial substances and the more we have in our arsenal the more opportunity for successfully treating inflammation-related conditions.

Immunomodulatory effect of riboflavin deficiency and enrichment - reversible pathological response versus silencing of inflammatory activation. - PubMed - NCBI

"...Mouse macrophage RAW 264.7 cells were cultured for 5 days in a medium with a riboflavin concentration corresponding to moderate riboflavin deficiency (3.1 nM), physiological state (10.4 nM), or vitamin pill supplementation (300 nM). On the third or fourth day of deprivation, the medium in some groups was supplemented with riboflavin (300 nM). Macrophages activation were assessed after LPS or zymosan stimulation. Short-term (5 days) riboflavin deprivation resulted in the pathological macrophages activation, manifested especially in a reduction of cell viability and excess release of tumor necrosis factor-α (TNF-α) and high-mobility group box 1 (HMGB1) protein. Moreover, the levels of inducible nitric oxide synthase (iNOS), nitric oxide (NO), heat shock protein (Hsp72), interleukin 1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and interleukin 10 (IL-10) decreased after riboflavin deprivation, but medium enrichment with riboflavin (300 nM) on the third or fourth day reversed this effect. In the riboflavin-supplemented group, LPS-stimulated macrophages showed lower mortality accompanied by higher Hsp72 expression, reduction of Toll-like receptor 4 (TLR4) and TNF-α, and elevation of NO, IL-6, and IL-10. Moreover, the TLR6, NO, iNOS, IL-1β, MCP-1, and the keratinocyte chemoattractant (KC) levels significantly decreased in the zymosan-stimulated groups maintained in riboflavin-enriched medium. We conclude that short-term riboflavin deficiency significantly impairs the ability of macrophages to induce proper immune response, while riboflavin enrichment decreases the proinflammatory activation of macrophage

 

[LeeLemonoil]

Severe toxic effect of methylene blue 1% on iris epithelium and corneal endothelium - PubMed

In vivo intracameral injection of methylene blue 1% induces extreme cytotoxicity, primarily on the corneal endothelium and iris epithelium.

pubmed.ncbi.nlm.nih.gov