Genipin protects against H(2)O(2)-induced oxidative damage in retinal pigment epithelial cells by promoting Nrf2 signaling

Oxidative stress serves a vital function in the pathogenesis of age-related macular degeneration (AMD); genipin (GP) possesses antioxidative properties. The present study aimed to investigate the effects of GP on retinal pigment epithelial (RPE) cells induced by H(2)O(2) and the underlying mechanism. ARPE-19 cells were subjected to H(2)O(2) treatment to induce oxidative damage. Cell viability was determined via an MTT assay. Reactive oxygen species (ROS) levels and cell apoptosis were detected by flow cytometry. Nuclear factor-erythroid 2-related factor-2 (Nrf2) signaling-associated and the expression of apoptosis-associated factors were measured using reverse transcription-quantitative polymerase chain reaction assay and western blotting. The results revealed that 200 µM H(2)O(2) and 30 µM GP were determined to be the optimal concentrations for subsequent experimentation. GP reversed the inhibitory effects of H(2)O(2) by promoting cell viability, attenuating ROS accumulation and cell apoptosis, and increased the expression of Nrf2, heme oxygenase-1 (HO-1) and NAD(P)H: Quinine oxidoreductase 1 (NQO1); Nrf2 silencing inhibited HO-1 and NQO1 expression. In addition, Nrf2 silencing enhanced the effects of H(2)O(2) by promoting ROS production and cell apoptosis. Compared with H(2)O(2), Nrf2 silencing further decreased the expression levels of B-cell lymphoma-2 (Bcl-2), but increased that of Bcl-2-associated X protein and cleaved-caspase-3. The results of the present study revealed that Nrf2 silencing attenuated the protective effects of GP on H(2)O(2)-induced injury in ARPE-19 cells by promoting apoptosis and oxidation. Collectively, GP attenuated oxidative damage induced by H(2)O(2) in ARPE-19 cells. Furthermore, the molecular mechanism may be associated with the Nrf2 signaling pathway. The findings of the present study nay provide insight into a potential therapeutic agent for the treatment of AMD.