Key result
Tanshinone IIA reduced prohibitin expression, apoptosis rate, and intracellular calcium concentration, and increased mitochondrial membrane potential in oxidative stress-injured myocardial cells.
Why the study?
Does tanshinone IIA reduce myocardial apoptosis and alter prohibitin expression in H2O2-induced oxidative stress in neonate rat myocardial cells?
Does tanshinone IIA reduce myocardial apoptosis and alter prohibitin expression in H2O2-induced oxidative stress in neonate rat myocardial cells?
Tanshinone IIA protects neonate rat myocardial cells from oxidative stress-induced apoptosis, potentially by reducing prohibitin expression.
Tanshinone IIA may attenuate oxidative myocardial injury in rats; hypothesis-generating for human cardioprotection pending clinical validation.
OBJECTIVE: To investigate the protective action of tanshinone IIA (TSN) on myocardial apoptosis induced by hydrogen peroxide (H2O2) and its effect on prohibitin (PHB) expression to probe the role of PHB in the oxidation stress of myocardial cells. METHODS: Primary cultured neonate rat myocardial cells were cultured with TSN (1 x 10(-4) mol/L) for 24 hours, and then the medium was supplemented with 200 micromol/L hydrogen peroxide for 2 h to initiate myocardial cell oxidative stress injury. PHB in myocardial cells was knocked down by small interfering RNA (siRNA), and the expression level of PHB was determined by western blot analysis. Flow cytometry was used to detect the apoptosis rate, intracellular calcium ion concentration ([Ca2+]i) and mitochondrial membrane potential (MMP). RESULTS: The PHB expression, [Ca2+]i and the apoptotic rate significantly increased, and the MMP significantly decreased in the oxidative stress group compared with the control. The PHB expression, apoptosis rate and [Ca2+]i decreased, and MMP increased significantly in the TSN group compared with the oxidative stress group. Compared with the siRNA negative control group, the PHB expression level in myocardial cells was down-regulated, and the apoptosis rate and [Ca2+]i increased, and MMP decreased significantly in the siRNA group. CONCLUSION: TSN can reduce PHB expression in oxidative stress-injured myocardial cells hence protecting the myocardial cells.
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Yang et al. (2010) studied Myocardial cell oxidative stress injury. Tanshinone IIA (TSN) vs. Oxidative stress group (H2O2 alone) and control was evaluated on PHB expression, apoptosis rate, intracellular calcium ion concentration, and mitochondrial membrane potential. Tanshinone IIA reduced prohibitin expression, apoptosis rate, and intracellular calcium concentration, and increased mitochondrial membrane potential in oxidative stress-injured myocardial cells.
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