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作 者:宋娟娟[1] 郭彩霞[1] 曾翔俊[2] 王红霞[2] 张立克[2] 杜凤和[1]
机构地区:[1]首都医科大学附属北京天坛医院,北京100050 [2]首都医科大学基础医学院
出 处:《山东医药》2013年第10期1-3,9,共4页Shandong Medical Journal
基 金:国家自然科学基金资助项目(30801217);北京市科技新星课题(2010B050)
摘 要:目的观察可溶性糖基化终产物受体(sRAGE)对缺氧/复氧(H/R)大鼠心肌细胞线粒体凋亡途径的影响。方法取大鼠心肌细胞培养72 h,以缺氧3 h、复氧2 h复制H/R模型,实验分为4组:对照组、对照+sRAGE组、H/R组、H/R+sRAGE组。以荧光探针JC-1方法检测线粒体膜电位,酯化钙黄绿素和氯化钴共孵育测定线粒体通透性转换孔(mPTP)开放,Western blot方法检测心肌细胞凋亡。结果与对照组比较,H/R组mPTP开放增多,线粒体膜电位去极化程度增加,凋亡率升高(P均<0.05);与H/R组比较,H/R+sRAGE组mPTP开放减少,线粒体膜电位去极化程度减轻,凋亡率下降(P均<0.05)。结论 sRAGE可通过抑制线粒体凋亡途径,拮抗心肌H/R损伤。Objective To observe the influence of soluble receptor of advanced glycation end products(sRAGE) on hypoxia/reoxygenation(H/R) myocardial pathway of mitochondria-apoptosis. Methods Neonatal rats cardiomyocytes were cultured for 72 h. The H/R injury model was replicated by cardiomyocytes hypoxia 3 11/reoxygenation 2 h. The cells were randomly divided into four groups : control group, control + sRAGE group, H/R group, and H/R + sRAGE group. Changes of mitochondrial membrane potential were detected by fluorescent probe called JC-1, esterification calcein and cobalt chlo- ride were incubated to detect the opening of the mitochondrial permeability transition pore(mPTP), the myocardial apopto- sis was detected with Westernblot. Results Compared with control group, H/R group could increase the opening of mPTP, the degree of depolarization of mitochondrial membrane potential and the rate of apoptosis ( all P 〈 0.05). Compared with H/R group, H/R-sRAGE group could reduce the opening of mPTP, lower the degree of depolarization of mitochondrial membrane potential and decrease the rate of apoptosis ( all P 〈 0.05 ). Conclusions sRAGE may inhibit the pathway of mitochondria-apoptosis to antagonize myocardial H/R injury.
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