Detailed Information and Research Results
GlauCaps® is a preparation designed to support baroprotective therapy of glaucomatous neuropathy. Glaucoma is a progressive neuropathy of the optic nerve, associated with changes in the phenotypes of the trabecular meshwork and lamina cribrosa of the sclera, and the secondary process of accelerated apoptosis of retinal ganglion cells due to neurotrophic deprivation. Transforming Growth Factor‑beta (TGF‑β), a cytokine, plays a key role in the biochemical pathomechanism of glaucomatous neuropathy, biochemically mediating the pathological remodeling of the extracellular matrix in the trabecular meshwork (TM) and the optic nerve head.
Effect on the trabecular meshwork of the iridocorneal angle
The tension of TM cells, the density of the extracellular matrix (ECM), and the compliance of the structures in the aqueous outflow angle regulate aqueous humor (AH) outflow, and thus determine intraocular pressure (IOP). TGF‑β has the ability to influence both the number and phenotype of TM cells, leading to increased resistance within the structures of the iridocorneal angle and secondary elevation of IOP.
TGF‑β1, by increasing the expression and production of α-smooth muscle actin (α‑SMA), induces a myofibroblast phenotype in TM cells. These phenotypically altered TM cells, containing highly organized actin fibers called stress fibers, exhibit functional characteristics of smooth muscle-like cells (SMLC). Due to their contractile ability and the connection of their cytoskeleton to the ECM, SMLCs actively regulate aqueous humor outflow at the level of the trabecular meshwork. TGF‑β1 directly stimulates SMLC contraction. It also decreases the expression of matrix GLA protein (MGP), increasing TM stiffness and reducing the efficiency of the trabecular outflow pump.
TGF‑β2 reduces the TM cell population by promoting apoptosis and inhibiting proliferation. It induces a secretory phenotype in TM cells, leading to increased hydrostatic resistance of the trabecular meshwork through enhanced synthesis of extracellular matrix proteins, primarily collagen, within the ECM.
Effect on the lamina cribrosa of the sclera
TGF‑β plays a key role in the pathognomonic phenotypic changes of the lamina cribrosa of the sclera (LCS) associated with glaucomatous neuropathy. In the eye, lamina cribrosa cells and trabecular meshwork cells are the most phenotypically and genotypically similar cell types, with genotypic similarity exceeding 97% [Steely T.H., Exp Eye Res. 2000]. Their similarity also extends to their embryogenesis—both cell populations originate from the neural crest and begin forming from the 12th week of fetal development. TGF‑β1 induces the transformation of LCS cells (analogous to TM cells) toward a smooth muscle-like cell (SMLC) phenotype. These phenotypically altered LCS cells play a central role in the pathological remodeling of the lamina cribrosa structures, which underlies secondary neurotrophic deprivation of retinal ganglion cells and accelerates their apoptosis, leading to glaucomatous neuropathy.
GlauCaps® has been shown, both experimentally and at clinically significant levels, to inhibit the pathological effects of TGF‑β on trabecular meshwork cells and lamina cribrosa cells.
GlauCaps® – through its protective effects on trabecular meshwork cells and lamina cribrosa cells, supports the neuroprotection of retinal ganglion cells during therapy for ocular hypertension and glaucomatous neuropathy.
Research Results on the Efficacy of GlauCaps®
Genistein
Genistein is a chemical compound from the isoflavone/phytochemical estrogen group, showing strong affinity for β‑estrogen receptors. It increases cell viability and inhibits the pathological effects of TGF‑β on human trabecular meshwork cells (HTMC) and lamina cribrosa cells (LC). This therapeutic effect is observed at genistein concentrations above 2 mg/L, reaching a maximum in the 10–15 mg/L range.
Oral supplementation with GlauCaps® results in a therapeutically significant concentration of 13.6 ± 3 mg/L of genistein in the aqueous humor of eyes in patients with primary open‑angle glaucoma (POAG) (control group: 0.36 ± 0.3 mg/L).
Fig. 1. Concentration of GlauCaps® Genistein in the aqueous humor of the eye after oral supplementation with GlauCaps®.
Fig. 2. Concentration of Genistein in the aqueous humor of the eyes in the control group.
At experimentally confirmed and clinically significant levels, this concentration of GlauCaps® Genistein increases cell viability (Fig. 3) and inhibits the pathological effects of TGF‑β1 (Fig. 4) and TGF‑β2 (Fig. 5) on HTMCs, maintaining homeostasis of aqueous humor outflow pathways and promoting a baroprotective effect (Wiederholt M., Invest. Ophth. Vis. Sci. 1998).
Due to the genotypic and phenotypic similarity between HTMCs and lamina cribrosa cells, GlauCaps® Genistein also exerts a protective effect on the lamina cribrosa, supporting the neuroprotection of retinal ganglion cells.
Fig. 3. Effect of GlauCaps® Genistein concentration on the viability of human trabecular meshwork cells (HTMC).
Fig. 4. Inhibitory effect of GlauCaps® Genistein on TGF‑β1‑induced myofibroblastic transformation of human trabecular meshwork cells (HTMC).
Fig. 5. Inhibitory effect of GlauCaps® Genistein on TGF‑β2‑induced myofibroblastic transformation of human trabecular meshwork cells (HTMC) and collagen production.
EGb 761
A standardized extract of Ginkgo biloba consists of flavonoids, mainly quercetin and rutin, and terpenoids, primarily bilobalide and ginkgolides.
The neuroprotective mechanism of action of EGb 761, which reduces the risk of progression of glaucomatous neuropathy, is based on improving ocular blood flow, inhibiting glutamate‑related neurotoxicity, exerting antioxidant effects, and inhibiting platelet-activating factor (PAF), nitric oxide (NO), and lipid peroxidation.
EGb 761 enhances ocular blood flow by improving the rheological properties of erythrocytes and reducing blood viscosity without affecting coagulation parameters. It strongly inhibits the release of glutamate—one of the main chemicals driving apoptosis of retinal ganglion cells. EGb 761 also potently inhibits PAF activity and NO release, reducing platelet aggregation, inhibiting neutrophil degranulation, and decreasing free radical production. The flavonoids in EGb 761 exert strong antioxidant effects, and inhibition of lipid peroxidation in erythrocytes contributes to stabilization of vascular endothelium.
ECGC
Epigallocatechin Gallate (EGCG)
The neuroprotective mechanism of EGCG, which reduces the risk of progression of glaucomatous neuropathy, is based on improving the function of the inner layers of the retina, achieved through antioxidant activity, restoration of retinal and optic nerve microcirculation integrity, and stabilization of the collagen structure of the eye.
Improved function of retinal ganglion cells (RGCs) is linked to mitochondrial protection through antioxidant effects. EGCG—the most potent natural antioxidant—protects RGCs by directly scavenging free radicals and enhancing the activity of endogenous antioxidant systems.
The vasoprotective effect of EGCG is based on reducing levels of VEGF, bFGF, and HIF‑1α, while its anti-inflammatory activity, which stabilizes collagen structure, is achieved by reducing NF‑κB and CRP activity.
GlauCaps® Ingredients
Ingredients: Green tea leaf extract (Camellia sinensis O. Ktze.), bulking agents: microcrystalline cellulose, hydroxypropyl methylcellulose, Ginkgo biloba leaf extract (Ginkgo biloba L.), Japanese pagoda tree fruit extract (Sophora japonica L.), zinc oxide (zinc), purified water, gelling agent: carrageenan, anti-caking agents: magnesium salts of fatty acids, silicon dioxide, gelling agent: potassium acetate, colorant: copper chlorophyllin complexes, sodium selenite (selenium). Do not use in case of hypersensitivity or allergy to any of the product’s ingredients.
Buy GlauCaps®
GlauCaps®
14.00 €The world’s first dietary supplement supporting glaucoma therapy.
Take one capsule daily!
Polish product (EU)
The world’s first fully Polish supplement to support glaucoma therapy
Cruelty free
Product not tested on animals.