人参皂甙 Rb1对大鼠缺血再灌注心肌细胞Bcl-2、Bax、Bad、Fas基因表达的影响

目的观察人参皂甙Rb1对缺血再灌注心肌细胞Bcl-2、Bax、Bad、Fas基因表达的影响.方法结扎/松解Wistar大鼠左冠状动脉前降支,建立大鼠缺血再灌注动物模型,免疫组化法检测Bcl-2、Bax、Bad、Fas基因的蛋白表达,并利用图象分析系统测量蛋白阳性表达区域平均光密度值,进行定量分析.结果缺血再灌注组及Rb1治疗组Bcl-2、Bax、Bad、Fas基因的表达较假手术组明显增加(P<0.05), Rb1治疗组Bcl-2的表达与缺血再灌注组比较无明显差异(P>0.05),而Bax、Bad、Fas的表达明显下降(P<0.05),人参皂甙Rb1治疗组Bcl-2/Bax、Bcl-2/Bad以及Bcl-2/Fas比值均较假手术组与缺血再灌注组明显增加.结论人参皂甙Rb1治疗可以抑制缺血再灌注心肌细胞中促凋亡基因Bax、Bad、Fas的表达,并使Bcl-2/Bax、Bcl-2/Bad以及Bcl-2/Fas比值增加.

EFFECT OF GINSENOSIDE-Rb1 ON Bcl-2, Bax, Bad AND Fas GENES EXPRESSION OF CARDIOMYOCYTES AFTER ISCHEMIA AND REPERFUSION IN RATS

Objective To observe the effect of ginsenoside Rb 1 on the gene expression of Bcl-2, Bax, Bad and Fas in cardiomyocytes of rats after ischemia (30min) and reperfusion (6h) .Method The ischemia/ reperfusion heart model was established by ligating/loosening the left anterior descending branch of coronary artery in Wistar rats. The protein expression of Bcl-2, Bax, Bad and Fas genes was studied by immunohistochemical staining, and the mean optical density (OD) values of the positive fields of protein expression were quantitatively examined by image analysis system. Result The gene expression of Bcl-2, Bax, Bad and Fas was increased significantly in the ischemia/reperfusion group and ginsenoside Rb 1-treated group as compared with that of the sham-operation group (P<0.05). There were no significant difference in the Bcl-2 gene expression between the ginsenoside Rb 1 treated group and ischemia/reperfusion group (P>0.05), but the gene expression of Bax, Bad, and Fas were decreased significantly in the ginsenoside Rb 1 treated group as compared with that of the ischemia/reperfusion group (P<0.05). The protein expression ratios of Bcl-2/Bax, Bcl-2/Bad and Bcl-2/Fas were increased significantly in the ginsenoside Rb 1 treated group as compared with those of the ischemia/reperfusion group and sham-operation group.Conclusion Ginsenoside Rb 1 can significantly inhibit the expression of pro-apoptotic Bax, Bad and Fas genes and raise the ratios of Bcl-2/Bax, Bcl-2/Bad and Bcl-2/Fas in cardiomyocytes.