摘要Summary: To observe the effect of ginsenoside Re on cardiomyocyte apoptosis and Bcl-2/Bax geneexpression after ischemia (30 min) and reperfusion (6 h) in rats and to elucidate the possiblemechanisms of ginsenoside Re on inhibition of cardiomyocyte apoptosis, the ischemia/reperfusionheart model was established by ligating the left anterior descending branch of coronary artery inWistar rats. The apoptotic cardiomyocytes were confirmed by transmission electron microscopyand counted by in situ nick end labeling (TUNEL) method and light microscopy. The mRNA andprotein expression of Bcl-2 and Bax genes were studied by in situ hybridization and immunohis-tochemical staining. Mean optical density (OD) value of the positive fields of mRNA and proteinexpression 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 groupand weren't observed in the sham-operation group by transmission electron microscopy; (2) Thenumbers of the apoptotic cells were 134. 45±45.61/field in the ischemia/reperfusion group, and90. 66±19.22/field in the ginsenoside Re-treated group. The differences was significant betweentwo groups(P＜0.01) ; (3) Gene expression of Bcl-2 and Bax were increased significantly in the is-chemia/reperfusion group and ginsenoside Re-treated group when compared with the sham-opera-tion group. There was no significant difference in the gene expression of Bcl-2 between the gin-senoside Re-treated group and ischemia/reperfusion group (P＞0. 05), but gene expression of Baxwas 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 ginseno-side Re-treated group when compared with the ischemia/reperfusion group and sham-operationgroup. These findings suggest that myocardial ischemia-reperfusion can induce cardiomyocyteapoptosis, and ginsenoside Re can significantly inhibit car diomyocyte apoptosis induced by ischemi-a-reperfusion in rats. It is concluded that ginsenoside Re inhibits cardiomyocyte apoptosis by in-hibiting expression of pro-apoptotic Bax gene and raising the ratio of Bcl-2/Bax.