Protective effects of aucubin on H₂O₂-induced apoptosis in PC12 cells

The present study investigated the neuroprotective effects of aucubin on hydrogen peroxide (H₂O₂)-induced apoptosis in PC12 cells. Exposure of PC12 cells to 0.25 mm H₂O₂ induced a leakage of lactate dehydrogenase and decreased cell viability, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In a dose over 0.1 mm, aucubin increased PC12 cellular viability and markedly attenuated H₂O₂-induced apoptotic cell death. Quantitation of apoptosis by flow cytometry indicated that aucubin inhibited H₂O₂-induced apoptosis in PC12 cells. Nuclear damage was alleviated by aucubin, as shown by Hoechst staining. In addition, the levels of malondialdehyde were reduced and the activity of superoxide dismutase, catalase and glutathione peroxidase was augmented in these cells. These results indicated that aucubin inhibited H₂O₂-induced apoptosis in PC12 cells through regulation of the endogenous oxidant-antioxidant balance. Our results suggest that aucubin is a potential protective agent for the treatment of oxidative-stress-induced neurodegenerative disease.