| The dissertation studied the mechanism of the protective effects of Hyperoside from oxidative stress in vitro. The signaling transduction pathways of Hyperoside pharmacological functions, including mitochondrial protective effect, apoptotic inhibitory impact, and mitochondrial regulatory function were demonstrated in the study.After exposure to the oxidative agent tert-butylhydroproxide (TBHP), then oxidative damage occured, it caused cell death eventually. Hyperoside inhibited TBHP-induced cell injury, and the antioxidative ability was stronger than that of N-acetylcysteine (NAC). All the results indicated that Hyperoside decreased the concentration of MDA and enhanced the activity of SOD. The protective effect of Hyperoside from TBHP-induced cell injury was related to mitochondrial function; Hyperoside improved and partially renewed the mitochondrial membrane potential (ΔΨ), these subsequently increased mitochondrial redox ability. Furthermore, the release of pro-apoptosis factor cytochrome c from mitochondria was blocked by Hyperoside-treatment. In addition, Hyperoside could regulate the location of Bcl-2 family protein, and reversed TBHP-induced apoptosis. Therefore, Hyperoside inhibited oxidative stress induced apoptosis through improving mitochondrial function and regulating Bcl-2 family protein.In conclusion, Hyperoside effectively protected oxidative stress-induced cell injury and improved the mitochondrial function. |
