Neuroprotective effects of torularhodin against H2O2-induced oxidative injury and apoptosis in PC12 cells

The neuroprotective effects of torularhodin against oxidative injury and apoptosis in PC12 cells, as well as the related mechanisms, were investigated. The results showed that torularhodin significantly reduced lactate dehydrogenase (LDH) release and malondialdehyde (MDA) production, meanwhile increased the activities of antioxidant enzymes, which were assessed by enzyme linked immunosorbent assay. The presence of torularhodin attenuated H2O2-induced apoptosis which was proven by flow cytometric detection of Ca2+ influx inhibition and the mitochondrial membrane potential (MMP) reduction. Furthermore, the oxidative injury produced by H2O2 was mitigated by torularhodin pretreatment via down-regulation of GSK-3β and Keap1 genes while up-regulating the expressions of Nrf2, HO-1 and NQO1 genes. The neuroprotective effects of torularhodin against oxidative injury and apoptosis appeared to be associated with the synergistic effect of mitochondria-mediated pathway and GSK-3β/ Nrf2 signaling pathway. These findings demonstrated that torularhodin could be considered as a neuroprotective agent against H2O2-induced oxidative stress.