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.