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目的 :观察人参皂甙Re(以下简称Re)对缺血再灌注心肌细胞凋亡及Fas基因表达的影响 ,探讨Re抑制心肌细胞凋亡的可能机制。方法 :结扎Wistar大鼠左冠状动脉前降支 ,建立大鼠缺血再灌注动物模型 ;采用透射电镜、缺口末端标记法检测心肌凋亡细胞 ,利用光学显微镜进行细胞计数 ;原位杂交及免疫组化分别检测Fas基因mRNA及蛋白的表达 ,并利用图像分析系统测量阳性表达区域平均光密度值 ,进行定量分析。结果 :①透射电镜发现缺血再灌注组缺血区出现心肌凋亡细胞 ,假手术组未发现心肌凋亡细胞 ;②缺血再灌注组心肌细胞凋亡数为 (134.4 5± 4 5 .6 1)个 /视野 ,Re治疗组细胞凋亡数 (90 .6 6± 19.2 2 )个 /视野 ,两组间差异有非常显著性意义 (P<0 .0 1) ;③原位杂交及免疫组化检测均发现Fas基因的表达缺血再灌注组较假手术组明显增加 (P <0 .0 1) ,Re治疗组较缺血再灌注组明显下降 (P <0 .0 5 )。结论 :心肌缺血再灌注诱导心肌细胞凋亡 ,Re治疗则可以显著减少缺血再灌注心肌细胞的凋亡。Re通过抑制Fas基因的表达而抑制心肌细胞凋亡
Objective: To observe the effect of ginsenoside Re (abbreviated as Re) on myocardial apoptosis and Fas gene expression after ischemia-reperfusion, and to explore the possible mechanism of Re inhibiting myocardial cell apoptosis. METHODS: Wistar rat left anterior descending coronary artery was ligated to establish a rat model of ischemia-reperfusion. Apoptotic myocytes were detected by transmission electron microscopy and nick end labeling. The cells were counted by light microscopy; in situ hybridization and immunization. The expression of Fas mRNA and protein was detected separately, and the average optical density of the positive expression area was measured using an image analysis system for quantitative analysis. RESULTS: 1 Apoptotic cells were found in the ischemic area of ischemia-reperfusion group by transmission electron microscope. No apoptotic cells were found in the sham-operated group. 2 The number of myocardial cell apoptosis in the ischemia-reperfusion group was (134.4 5± 4 5. 6 1)/field, number of apoptotic cells in the Re treatment group (90.66 ± 19.2 2)/field, significant difference between the two groups (P < 0.01); 3 in situ hybridization and immunization The expression of Fas gene in the ischemic reperfusion group was significantly higher than that in the sham group (P < 0.01). The Re group was significantly lower than that in the ischemia-reperfusion group (P <0.05). Conclusion : Myocardial apoptosis induced by myocardial ischemia and reperfusion, Re treatment can significantly reduce the apoptosis of myocardial cells after ischemia and reperfusion. Re inhibits cardiomyocyte apoptosis by inhibiting Fas gene expression