Study of anti-myocardial cell oxidative stress action and effect of tanshinone IIA on prohibitin expression
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Ping Yang1, Yu-Hua Jia, Jie Li
1Southern Medical University, Guangzhou 510515, China.
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.
Insights
Tanshinone IIA (TSN) protects myocardial cells from hydrogen peroxide (H2O2) induced oxidative stress by reducing prohibitin (PHB) expression. This finding highlights TSN
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Oxidative Stress Research
Background:
- Myocardial apoptosis is a key pathological process in cardiovascular diseases.
- Oxidative stress, induced by agents like hydrogen peroxide (H2O2), significantly contributes to myocardial injury.
- Prohibitin (PHB) is implicated in cellular stress responses, but its role in myocardial oxidative stress requires further elucidation.
Purpose of the Study:
- To investigate the protective effects of tanshinone IIA (TSN) against H2O2-induced myocardial apoptosis.
- To examine the impact of TSN on prohibitin (PHB) expression in oxidative stress-injured myocardial cells.
- To explore the role of PHB in myocardial cell response to oxidative stress.
Main Methods:
- Primary neonatal rat myocardial cells were subjected to oxidative stress using H2O2.
- Cells were treated with TSN or had PHB expression reduced using small interfering RNA (siRNA).
- Apoptosis rate, intracellular calcium ion concentration ([Ca2+]i), mitochondrial membrane potential (MMP), and PHB expression (Western blot) were assessed.
Main Results:
- Oxidative stress increased PHB expression, apoptosis, and [Ca2+]i, while decreasing MMP.
- TSN treatment reversed these effects, reducing apoptosis, [Ca2+]i, and increasing MMP.
- siRNA-mediated knockdown of PHB exacerbated apoptosis and [Ca2+]i, and decreased MMP, indicating PHB's protective role.
Conclusions:
- Tanshinone IIA (TSN) demonstrates significant cardioprotective effects against oxidative stress.
- TSN mitigates myocardial apoptosis by modulating prohibitin (PHB) expression.
- PHB plays a crucial role in the myocardial cell's response to oxidative stress injury.