LAUSR

Glaucoma is a chronic neurodegenerative disease which produces damage to the optic nerve and causes sightlessness. Current remains lack of effective method for glaucoma. Lycium barbarum polysaccharides (LBPs) have pleiotropic effects on various diseases. However, the effect of LBPs on glaucoma remains unclear. The study aimed to clarify the protective effect of LBPs against hydrogen peroxide (H2O2)-induced oxidative damage in human trabecular meshwork (HTM) cells. HTM cells were exposed to H2O2 (0-400 μM) for 24 h to construct an oxidative damage model. Then, the different concentrations of LBPs (0-500 μg mL-1) were used to pre-treated HTM cells, and cell viability, apoptosis, protein levels of pro-/cleaved-caspase-3 and pro-/cleaved-caspase-9, and reactive oxygen species (ROS) generations were detected. MicroRNA (miR)-4295 inhibitor and its control were transfected into HTM cells, and the biological functions of miR-4295 were assessed in H2O2 and LBPs treated cells. Phosphatidylinositol 3-kinase (PI3K)/protein Kinase B (AKT) and extracellular regulated protein kinases (ERK) pathways were determined by western blot assay. LBPs significantly promoted cell viability, reduced apoptosis, declined cleaved-caspase-3/-9 and ROS level in HTM cells after H2O2 administration. MiR-4295 expression was up-regulated in H2O2 and LBPs treated cells. The protective effect of LBPs on H2O2-injured HTM cells was obviously reversed by miR-4295 inhibition. LBPs activated PI3K/AKT and ERK signaling pathways through up-regulation of miR-4295 in H2O2-injured HTM cells. These data demonstrated that LBPs alleviated H2O2-induced injury by up-regulation of miR-4295 in HTM cells, indicating the protective effect of LBPs on HTM cells against oxidative damage.