Effect of myricetin on primary open-angle glaucoma

Abstract

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. 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. 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. The observations of the study illustrate the protective effects of myricetin in glaucomatous TM cells.