【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。更多还原

【Abstract】 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 h/ 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 chloride were incubated to detect the opening of the mitochondrial permeability transition pore(mPTP),the myocardial apoptosis 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.更多还原