首页> 中文期刊> 《中西医结合心脑血管病杂志》 >丹参饮预处理对心肌缺血/再灌注损伤大鼠的心肌保护作用研究

丹参饮预处理对心肌缺血/再灌注损伤大鼠的心肌保护作用研究

         

摘要

Objective To assess the effect of Danshen decoction (DSD) preconditioning against myocardial ischemia/reperfusion injury (MIRI) in rats, and explore the mechanism.Methods Wistar rats were randomly divided into normal control group, ischemia/reperfusion (I/R) model group, cyclosporine A preconditioning I/R group, and DSD preconditioning I/R group.After gavaged for 1 week, the myocar-dial ischemia/reperfusion model was induced by ligation of the anterior descending coronary artery for 30 min/reperfusion for 120 min.Infarct size was assessed by triphenyl tetrazolium chloride (TTC) staining.The mitochondrial ultrastructure was observed by transmissionelectron microscope (TEM).The response of isolated mitochondria to Ca2+was measured as an index of mitochondrial permeability tran-sition pore opening.Results Compared with I/R model group, the infarction size in cyclosporine A preconditioning group and DSD pre-conditioning I/R group were reduced (P <0.05).Compared with the normal control group, the isolated myocardial mitochondria respon-ding to Ca2+was swollen, and the ratio of absorbance decreased rapidly in the I/R group (P <0.05);compared with the I/R modelgroup, the decrease of absorbance of mitochondria induced by Ca2+was partially recovered in cyclosporine A preconditioning group andDSD preconditioning group (P <0.05).TEM showed that the myocardial mitochondria was significantly swollen in the I/R group com-pared with the normal control group, while they were attenuated in cyclosporine A preconditioning group and DSD preconditioning groupcompared with the I/R group.Conclusion DSD preconditioning has cardioprotection against MIRI in rats, and its mechanism may be re-lated to inhibiting the opening of mitochondrial permeability pore, and attenuating myocardial mitochondrial swelling.%目的 观察丹参饮对心肌缺血/再灌注损伤(MIRI)大鼠的心肌保护作用,并探讨其作用机制.方法 将清洁级Wistar大鼠随机分为空白对照组、缺血/再灌注(I/R)模型组、环孢菌素预处理I/R组和丹参饮预处理I/R组.各组给予相应的药物连续灌胃1周结束后,通过结扎大鼠冠状动脉前降支30 min/复灌120 min复制心肌缺血/再灌注模型.使用2,3,5-三苯基氯化四氮唑(TTC)染色法观察各组心肌梗死面积,透射电镜观察心肌线粒体超微结构,运用Ca2+诱导的线粒体肿胀程度法观察心肌线粒体通透性转换孔开放的情况.结果 与I/R模型组比较,环孢菌素预处理I/R组和丹参饮预处理I/R组心肌梗死面积均明显缩小(P <0.05);与空白对照组比较,I/R模型组大鼠心肌线粒体在Ca2+诱导下,线粒体肿胀、吸光度比值下降迅速(P <0.05);而与I/R模型组相比,环孢菌素预处理I/R组和丹参饮预处理I/R组大鼠心肌线粒体在Ca2+诱导下吸光度下降速度较I/R模型组明显改善(P <0.05).透射电镜观察发现:I/R模型组较空白对照组大鼠心肌线粒体明显肿胀,而环孢菌素预处理I/R组和丹参饮预处理I/R组较I/R模型组明显改善.结论 丹参饮预处理对MIRI具有一定的心脏保护作用,其机制可能与抑制大鼠心肌线粒体细胞膜转换孔开放、减少心肌线粒体肿胀相关.

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