Ginsenoside‑Rb3 protects the myocardium from ischemia‑reperfusion injury via the inhibition of apoptosis in rats

Liu,Xiaomin; Jiang,Yichuan; Yu,Xiaofeng; Fu,Wenwen; Zhang,Hong; Sui,Dayun

doi:10.3892/etm.2014.2007

December-2014 Volume 8 Issue 6

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December-2014 Volume 8 Issue 6

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Article

Ginsenoside‑Rb3 protects the myocardium from ischemia‑reperfusion injury via the inhibition of apoptosis in rats

Authors:
- Xiaomin Liu
- Yichuan Jiang
- Xiaofeng Yu
- Wenwen Fu
- Hong Zhang
- Dayun Sui
View Affiliations / Copyright

Affiliations: Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China
Pages: 1751-1756
|
Published online on: October 7, 2014

https://doi.org/10.3892/etm.2014.2007
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Abstract

Ginsenoside‑Rb3 (G‑Rb3) has been previously demonstrated to attenuate myocardial ischemia‑reperfusion injury (MIRI). The aim of the present study was to investigate this further and determine whether G‑Rb3 protects the myocardium from ischemia‑reperfusion injury via the inhibition of apoptosis. Adult male Sprague Dawley rats were randomly divided into four groups: Sham, MIRI, G‑Rb3 treatment (orally, 20 mg/kg) and ischemic postconditioning (as the positive control). The drug or placebo treatment was administered to the rats once a day for three consecutive days, and MIRI was then induced by subjecting the rats to left anterior descending coronary artery ligation for 30 min and reperfusion for 2 h. The results showed that G‑Rb3 treatment significantly reduced the number of apoptotic cells in the myocardium and the expression of B‑cell lymphoma 2‑associated X protein, and increased the expression of B‑cell lymphoma 2. The activities of aspartate aminotransferase, lactate dehydrogenase and creatine kinase‑MB in the serum were also reduced significantly by the G‑Rb3 treatment. These findings suggest that G‑Rb3 inhibits apoptosis in the early stage of MIRI, and attenuates MIRI when the reperfusion continues. G‑Rb3 was also shown to significantly reduce the level of malondialdehyde and increase the activity of superoxide dismutase in the myocardium, which suggests that attenuating reactive oxygen species accumulation and oxidative stress may be the major mechanism underlying the anti‑apoptotic effects of G‑Rb3. The release of inflammatory factors was significantly attenuated by G‑Rb3, which may also be associated with its anti‑apoptotic effects.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Ginsenoside‑Rb3 protects the myocardium from ischemia‑reperfusion injury via the inhibition of apoptosis in rats

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