Objective: To study the anti-apoptotic mechanism of tanshinoneⅡA and the function of prohibitin (PHB) on myocardial cell apoptosis induced by hydrogen peroxide(H2O2). Method: there were six groups of myocardial cells in the study: normal control group

oxidative stress group

tanshinoneⅡA group

siRNA group

siRNA+oxidative stress group

siRNA control group. Primary cultured neonate rat myocardial cells were cultured in medium with 200 μmol ·L-1 hydrogen peroxide

and the medium was supplemented with tanshinoneⅡA (1×10-4

5×10-5

1×10-5 mol ·L-1) in advance for 24 hours. PHB in myocardial cells was knocked down by small interfering RNA (siRNA) interference

and the expression level of PHB was determined by western blotting analysis. Flow cytometric analysis was used to detect apoptosis rate

i and mitochondrial membrane potential(MMP). Result: H2O2-mediated cell apoptosis resulted in activation of PHB

increasing of i

and decreasing of mitochondrial membrane potential. Tanshinone IIA profoundly prohibited myocardial cells apoptosis induced by hydrogen peroxide

and decreased i

and increased mitochondrial membrane potential in a dose dependent manner. Specific silence of PHB by siRNA down-regulated the expression level of PHB and increased of apoptosis rate and i

and decreased mitochondrial membrane potential. Conclusion: The results demonstrated that the activation of PHB is compensatory increased in myocardial cells against oxidative stress. tanshinone ⅡA could reduce the expression of PHB by attenuate the injury induced by oxidative stress.