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目的探讨人参皂甙Re(GSRe)对高儿茶酚胺大鼠心肌损伤的保护作用。方法采用异丙基肾上腺素(ISO)腹腔注射方法建立高儿茶酚胺大鼠模型。18只实验大鼠随机分为对照组、ISO组和GSRe治疗组(GSRe组)。记录各组大鼠心电图变化。取心肌组织分别行透射电镜检查、原位缺口末端标记(TUNEL)法检测和Fas、Bcl-2基因蛋白表达的免疫组织化学检测。结果与对照组比较,ISO组心率显著增快(P<0.01),且有室性心律失常发生;电镜下可见心肌细胞凋亡,心肌细胞凋亡指数及Fas、Bcl-2基因蛋白表达阳性指数均增加(Pa<0.01)。GSRe组较ISO组心率减慢,可逆转室性心律失常为窦性心律;电镜下核染色质边集浓缩缓解,心肌细胞凋亡指数显著下降(P<0.01)、Fas基因蛋白表达阳性指数显著下降(P<0.01)、Bcl-2基因蛋白表达阳性指数显著升高(P<0.01)。结论 GSRe可拮抗ISO诱导的大鼠心动过速,逆转室性心律失常,同时可下调Fas基因表达、上调Bcl-2基因表达,抑制大鼠心肌细胞凋亡。GSRe对高儿茶酚胺大鼠心肌损伤有保护作用。
Objective To investigate the protective effect of ginsenoside Re (GSRe) on myocardial injury induced by high catecholamine in rats. Methods High catecholamine rat model was established by intraperitoneal injection of isoproterenol (ISO). Twenty-eight experimental rats were randomly divided into control group, ISO group and GSRe treatment group (GSRe group). The changes of electrocardiogram in each group were recorded. The myocardial tissue was examined by transmission electron microscopy, TUNEL and immunohistochemistry of Fas and Bcl-2 protein respectively. Results Compared with the control group, the heart rate of ISO group increased significantly (P <0.01), and ventricular arrhythmia occurred. The apoptosis of cardiomyocytes, apoptotic index of cardiomyocytes and the positive expression of Fas and Bcl-2 protein (Pa <0.01). The heart rate of GSRe group was slower than that of ISO group, and the arrhythmia of ventricular arrhythmia was sinus rhythm. The concentration of nuclear chromatin was reduced and the apoptosis index of cardiomyocyte was significantly decreased under electron microscope (P <0.01). The positive expression of Fas gene protein was significant (P <0.01), and the positive expression of Bcl-2 protein was significantly increased (P <0.01). Conclusion GSRe can antagonize the ISO-induced rat tachycardia, reverse ventricular arrhythmia, reduce the expression of Fas gene and up-regulate the expression of Bcl-2 gene and inhibit the apoptosis of rat cardiomyocytes. GSRe has a protective effect on myocardial injury in high catecholamine rats.