黄芪甲苷通过调控PI3K/Akt信号通路减轻H2O2诱导的RPE细胞氧化应激与炎症损伤OA

To investigate the protective effects of Astragaloside Ⅳ(AS-Ⅳ)against H2O2-induced oxidative stress and in-flammatory injury in retinal pigment epithelial(RPE)cells,and to preliminarily elucidate its underlying mechanisms,an oxidative stress model was established by treating RPE cells with H2O2.The viability of cells was assessed using the CCK-8 assay,and membrane damage was evaluated by measuring LDH release.The levels of IL-6,TNF-α,and PGE2 were quantified by ELISA.Intracellular ROS accumulation was detected by ROS immunofluorescence staining,mitochondrial membrane po-tential was assessed using JC-1 staining,and the expression of PI3K/Akt pathway-related proteins and iNOS was analyzed by Western blot.The results were as follows:① CCK-8 assays showed that H2O2 treatment significantly reduced the viability of RPE cells,whereas AS-Ⅳ markedly improved the viability of H2O2-treated RPE cells in a dose-dependent manner;② H2O2 exposure significantly increased LDH release,IL-6,TNF-α,and PGE2 levels,as well as ROS accumulation and iNOS expres-sion,while AS-Ⅳ treatment significantly decreased LDH release and reduced IL-6,TNF-α,PGE2,ROS,and iNOS levels;③ H2O2 markedly decreased the red/green fluorescence ratio and reduced the relative expression of p-PI3K and p-Akt,whereas AS-Ⅳ significantly increased the red/green fluorescence ratio and promoted p-PI3K and p-Akt expression.Collectively,these findings suggest that AS-Ⅳ effectively alleviates H2O2-induced oxidative stress and inflammatory injury in RPE cells,poten-tially through reducing ROS levels,improving mitochondrial function,and activating the PI3K/Akt signaling pathway.