In the present study, we examined the hypothesis that TSM affords protection against H2O2-induced PC12 cells apoptosis by bcl-2- (an antiapoptotic protein-) mitochondria-ROS-INOS pathway, to investigate whether TSM could protect PC12 cells by the repetitive exposure to H2O2 against the apoptotic consequences of the subsequent oxidative insults and whether the H2O2-induced TSM adaptive cytoprotection related to the changes in mitochondrial membrane potential, ROS, INOS, and the bcl-2 expressions so as to explore a suitable candidate for neuroprotective therapy for the brain ischemia. The gene discussed is BCL2; the disease is brain ischemia.