依达拉奉对老年大鼠心肌缺血再灌注后线粒体功能的保护作用

发布时间：2018-03-18 16:42

本文选题：缺血再灌注　切入点：依达拉奉　出处：《中国老年学杂志》2015年15期 　论文类型：期刊论文

【摘要】：目的探讨依达拉奉(MCI-186)对老年大鼠心肌缺血再灌注(I/R)后线粒体的保护作用。方法 36只18个月龄大鼠随机分为假手术组、I/R组及治疗组,每组12只,结扎冠状动脉左前降支建立I/R模型,治疗组在再灌注开始时给予MCI-186静脉滴注(10 mg/kg)。再灌注180 min后,提取心肌组织,观察在透射电镜下线粒体形态变化,Western印迹检测凋亡相关蛋白Bcl-2、Bax及细胞色素C(cyt C)的表达水平,TUNEL法检测细胞凋亡程度,分光光度法检测线粒体膜通透性转换孔(m PTP)的开放程度。结果透射电镜下治疗组线粒体形态较I/R组规则,肿胀程度轻,嵴排列有序。治疗组Bcl-2表达明显高于I/R组,Bax及Cyt C表达明显低于I/R组(P0.05)。TUNEL染色治疗组心肌凋亡指数明显低于I/R组(P0.01)。治疗组m PTP在8~20 min开放程度明显低于I/R组(P0.05)。结论 MCI-186能够保护老年大鼠心肌I/R后的线粒体呼吸功能,维持线粒体膜的稳定性,进而减轻细胞凋亡。
[Abstract]:Objective to investigate the protective effect of Edaravone MCI-186 on mitochondria after myocardial ischemia reperfusion in aged rats. Methods Thirty-six 18-month-old rats were randomly divided into sham-operation group (n = 12) and treatment group (n = 12). I / R model was established by ligating the left anterior descending branch of coronary artery. In the treatment group, 10 mg / kg of MCI-186 was given intravenously at the beginning of reperfusion. After 180 min of reperfusion, myocardial tissue was extracted. The expression level of apoptosis-related protein Bcl-2P Bax and cytochrome cyt C were detected by Western blotting under transmission electron microscope and Tunel method was used to detect the degree of apoptosis. The opening degree of mitochondrial membrane permeability transition pore (mPTP) was measured by spectrophotometry. Results the mitochondrial morphology in the treatment group was less than that in the I / R group under transmission electron microscope, and the swelling degree was less than that in the I / R group. The expression of Bcl-2 in the treatment group was significantly higher than that in the I / R group, and the expression of Cyt C was significantly lower than that in the I / R group. The myocardial apoptotic index in the treatment group was significantly lower than that in the I / R group, and the opening degree of m PTP in the treatment group was significantly lower than that in the I / R group. Conclusion the expression of m PTP in the treatment group was significantly lower than that in the I / R group. MCI-186 can protect mitochondrial respiratory function after I / R in aged rats. Maintain the stability of mitochondrial membrane, and then reduce apoptosis.
【作者单位】：齐齐哈尔医学院附属三院老年科;
【分类号】：R965

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