中文摘要：

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72h，以缺氧3h、复氧2h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，Westernblot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。

英文摘要：

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.