Effect of ginsenoside Re on cardiomyocyte apoptosis and expression of Bcl-2/Bax gene after ischemia and reperfusion in rats

Abstract

To observe the effect of ginsenoside Re on cardiomyocyte apoptosis and Bcl-2/Bax gene expression after ischemia (30 min) and reperfusion (6 h) in rats and to elucidate the possible mechanisms of ginsenoside Re on inhibition of cardiomyocyte apoptosis, the ischemia/reperfusion heart model was established by ligating the left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were confirmed by transmission electron microscopy and counted byin situ nick end labeling (TUNEL) method and light microscopy. The mRNA and protein expression of Bcl-2 and Bax genes were studied byin situ hybridization and immunohistochemical staining. Mean optical density (OD) value of the positive fields of mRNA and protein expression was quantitatively examined by image analysis system. The results were as follows: (1) The apoptotic cardiomyocytes were found in ischemic fields in the ischemia/reperfusion group and weren’t observed in the sham-operation group by transmission electron microscopy; (2) The numbers of the apoptotic cells were 134.45±45.61/field in the ischemia/reperfusion group, and 90.66±19.22/field in the ginsenoside Re-treated group. The differences was significant between two groups (P<0.01); (3) Gene expression of Bcl-2 and Bax were increased significantly in the ischemia/reperfusion group and ginsenoside Re-treated group when compared with the sham-operation group. There was no significant difference in the gene expression of Bcl-2 between the ginsenoside Re-treated group and ischemia/reperfusion group (P>0.05), but gene expression of Bax was decreased significantly in the ginsenoside Re-treated group as compared with the ischemia/reperfusion group (P<0.01). The ratio of Bcl-2/Bax was increased significantly in the ginsenoside Re-treated group when compared with the ischemia/reperfusion group and sham-operation group. These findings suggest that myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and ginsenoside Re can significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats. It is concluded that ginsenoside Re inhibits cardiomyocyte apoptosis by inhibiting expression of pro-apoptotic Bax gene and raising the ratio of Bcl-2/Bax.

Keywords

ginsenoside Re / ischemia/reperfusion / cardiomyocyte apoptosis / Bcl-2/ Bax

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