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目的:研究生长激素对大鼠心肌缺血再灌注(myocardialischemiareper-fusion,MIR)后心肌细胞凋亡及其机制的影响。方法:24只大鼠随机分为3组,假手术组(仅手术24h)、MIR组、生长激素组,每组8只。后两组均缺血30min,再灌注24h,其中生长激素组的每只大鼠每天皮下肌注生长激素1U/kg,连续7d。前两组每只大鼠相应皮下肌注生理盐水0.5mL/d。以TUNEL法检测心肌细胞凋亡情况,DAB免疫组化法检测心肌细胞核NF-κB蛋白、心肌细胞胰岛素样生长因子-1(insulin-likegrowthfactor-1,IGF-1)的表达并进行心肌组织病理学检查。结果:大鼠MIR24h后心肌细胞凋亡指数明显上升犤MIR组(16.17±5.02)%,假手术组为0犦(t=9.111,P<0.05)。心肌细胞核NF-κB蛋白表达呈阳性染色指数(positiveindex,PI)明显升高犤MIR组(18.60±7.21)%,假手术组为0犦(t=7.297,P<0.05)。心肌病理检查见心肌缺血区呈大小不一的坏死孔灶,缺血心肌间有炎症细胞浸润,心肌排列不整齐(HE染色),而生长激素组心肌细胞凋亡率及心肌细胞核NF-κB蛋白PI明显好于MIR组(t=4.302,2.943,P<0.05)。生长激素组IGF-1着色强度明显高于另外两组(χ2=12.443,9.167,P<0.05),心肌细胞间炎症细胞也明显减少,坏死灶也少于MIR组。结论:生长激素可以减少MIR后心肌细胞凋亡及细胞核NF-κB?
Objective: To investigate the effect of growth hormone on cardiomyocyte apoptosis and its mechanism after myocardial ischemia and reperfusion (MIR) in rats. Methods: Twenty-four rats were randomly divided into three groups: sham operation group (24h for surgery only), MIR group and growth hormone group (n = 8). The latter two groups were ischemia 30min, reperfusion 24 hours, in which the growth hormone group, each rat subcutaneous muscle growth hormone 1U / kg, for 7 days. The first two groups corresponding to each rat subcutaneous muscle saline 0.5mL / d. The apoptosis of cardiomyocytes was detected by TUNEL method. The expression of nuclear factor-kappaB (NF-κB) and insulin-like growth factor-1 (IGF-1) were detected by DAB immunohistochemistry and myocardial histopathology an examination. Results: The apoptotic index of cardiomyocytes in MIR24h group was significantly higher than that in MIR group (16.17 ± 5.02%) and sham operation group (P0.01) (t = 9.111, P <0.05). The expression of NF-κB protein in cardiomyocytes increased significantly (P <0.05), the positive index (PI) increased significantly in MIR group (18.60 ± 7.21)% and sham group (P <0.05). Myocardial pathological examination showed ischemic area of myocardial necrosis in varying sizes necrosis, infiltration of inflammatory cells between ischemic myocardium, myocardial irregularly arranged (HE staining), while the growth hormone group of myocardial cell apoptosis and myocardial nuclear NF-κB Protein PI was significantly better than MIR group (t = 4.302,2.943, P <0.05). The staining intensity of IGF-1 in growth hormone group was significantly higher than that in other two groups (χ2 = 12.443,9.167, P <0.05), and the number of inflammatory cells in myocardial cells was significantly decreased. Conclusion: Growth hormone can reduce myocardial apoptosis and nuclear NF-κB after MIR.