| Abstrakt: |
Background: Primary open angle glaucoma (POAG) is the most common form of glaucoma, with a multifactorial etiology that results in retinal ganglion cell death and loss of vision. In this study, we assessed the effects of myricetin on the trabecular meshwork cells in POAG. Methods: In the in-vivo model, glaucoma was induced in Sprague-Dawley rats by injecting hyaluronic acid into the anterior chamber of the eye (every week for six-weeks). Treatment group rats were administered myricetin (25, 50 or 100 mg/ kg body weight via oral gavage) each day for of six weeks. Results: POAG TM cells exposed to myricetin (25, 50 or 100 μM) exhibited significantly lowered reactive oxidative species (ROS) levels and lipid peroxidation products. The expressions of transforming growth factors (TGFβ1/β2), vascular endothelial growth factor, and senescence markers (senescence associated-β-galactosidase, cyclin-dependent kinase inhibitors-p16 and p21) were substantially down-regulated in POAG TM cells exposed to myricetin. Myricetin effectively prevented IOP elevation in glaucoma-induced rats and decreased inflammatory cytokines (IL-1α, IL-1β, IL-6, Il-8, TNF-α) in the aqueous humor and POAG TM cells of glaucoma-induced rats. Conclusion: The observations of the study illustrate the protective effects of myricetin in glaucomatous TM cells. [ABSTRACT FROM AUTHOR] |
