Quercetin Protects Retina External Barrier from Oxidative stress Injury by Promoting Autophagy.

Age-related macular degeneration (AMD) is the primary cause of irreversible severe visual loss among the elderly globally. Oxidative stress acts as a vital role in the pathogenesis of dry AMD, during which cells activate the autophagic process to avoid further damage. It is well known that oxidative stress damage happened in retinal pigment epithelial cells (RPE) could disrupt the blood outer-retinal barrier (OBRB) and thus reduce the expressions of tight junction proteins and lead to its abnormal distribution. Recent research has proven that if we can improve autophagy, alleviate cellular senescence and inhibit bizarre retinal immune-inflammation responses, It may be feasible to postpone the development of AMD and to obtain better clinical results. Therefore, our research focuses on improving the level of autophagy. Quercetin has been purported to be a novel and easy cytoprotective agent for its efficiency in opposition to RPE cell death induced by oxidative stress. However, the effects of quercetin on the OBRB during oxidative stress remain undefined. The present study explored the biological functions and effects of quercetin on oxidative stress induced by H2O2 and its underlying mechanisms in the OBRB. We demonstrated that quercetin could protect human retinal pigment epithelial cells barrier-related proteins from oxidative stress via upregulating autophagy response. The outcomes offer a molecular foundation for the application of quercetin management in the treatment of AMD.