Abstract
Cerebral ischemia reperfusion (I/R) injury is a main pathogenesis of ischemic stroke, which involves cell oxidative stress, mitochondrial dysfunction and apoptosis. The aim of this study was to explore the effects of icariside II (ICS II) on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced PC12 cell injury. The results showed that ICS II ameliorated OGD/R-induced PC12 cells injury in a dose-dependent manner, evidenced by the increase of cell viability and the decrease of LDH leakage. Additionally, ICS II not only attenuated the reactive oxygen species (ROS), but also the overproduction of mitochondrial ROS, as well as recovered the mitochondrial membrane potential (MMP). Furthermore, results of western blot demonstrated that OGD/R accelerated cell oxidative stress and apoptotic along with reduced in nucleus-Nrf2, NQO-1, HO-1, Bcl-2 protein levels, and increased Keap1, Bax and cleaved Caspase-3 protein level, whereas ICS II reversed these changes. Interestingly, ICS II also restrain the OGD/R-induced decreased in SIRT3 and IDH2 expressions. All in all, this study indicated that ICS II alleviates OGD/R-induced PC12 cell injury, and its underlying mechanisms are associated with regulation of Nrf2/SIRT3 signaling pathway.
