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目的:探讨外源性肝细胞生长因子(hepatocytegrowthfactor,HGF)对心肌梗死后心肌细胞凋亡及左室重塑的影响。方法:将56只新西兰兔随机分为4组:假手术组、假手术+HGF组、对照组和干预组。结扎左冠状动脉前降支复制急性心肌梗死模型。干预组静脉注射给予HGF2mg/(kg·12h),4周后测心功能、左室重塑指标,取出心脏,梗死区/缺血区重量比为梗死范围。TUNEL法染色检测细胞凋亡。Westernblot法测定凋亡蛋白Bcl-2的表达。结果:与假手术组相比,对照组的左室舒张末容积、左室相对重量、左室壁厚度均显著升高(t=3.598,2.348,2.324,P<0.05～0.01),左室缩短分数(leftventricularfractionofshortening,LVFS)、左室射血分数(leftventricularejectionfraction,LVEF)均显著降低(t=4.311,3.330,P<0.01)。HGF干预组LVESV,LVEDV显著低于对照组(t=2.810,2.449,P<0.01);LVFS及LVEF均显著升高。HGF干预组细胞凋亡率、心肌梗死范围均低于对照组(t=2.302,2.344,P<0.01)。左室腔直径与心肌细胞凋亡率呈正相关(r=0.801,P<0.01)。干预组梗死心肌周围bcl-2表达(灰度值1.37)显著高于对照组(灰度值0.17)(t=21.043,P<0.01)。结论:HGF能减少心肌梗死范围、降低心肌细胞凋亡率并能限制心肌梗死后的左室重塑,改善心功能,其作用机制可能与其抗凋
Objective: To investigate the effect of exogenous hepatocyte growth factor (HGF) on cardiomyocyte apoptosis and left ventricular remodeling after myocardial infarction. Methods: 56 New Zealand white rabbits were randomly divided into 4 groups: sham operation group, sham operation + HGF group, control group and intervention group. Ligation of left anterior descending coronary artery for acute myocardial infarction model. The intervention group received intravenous injection of HGF 2 mg / (kg · 12 h). After 4 weeks, the cardiac function and left ventricular remodeling index were taken and the heart was removed. The weight ratio of infarct area to ischemic area was the infarction area. TUNEL staining was used to detect apoptosis. Western blotting was used to detect the expression of Bcl-2. Results: Compared with the sham operation group, left ventricular end diastolic volume, left ventricular relative weight and left ventricular wall thickness were significantly increased in the control group (t = 3.598, 2.348, 2.324, P <0.05-0.01) Left ventricular ejection fraction (LVFS) and left ventricular ejection fraction (LVEF) were significantly decreased (t = 4.311, 3.330, P <0.01). LVESV and LVEDV in HGF intervention group were significantly lower than those in control group (t = 2.810, 2.499, P <0.01); LVFS and LVEF were significantly increased. HGF intervention group apoptosis rate, myocardial infarction range were lower than the control group (t = 2.302,2.344, P <0.01). The diameter of left ventricular cavity was positively correlated with the rate of cardiomyocyte apoptosis (r = 0.801, P <0.01). The expression of bcl-2 in infarction myocardium (gray value 1.37) in intervention group was significantly higher than that in control group (gray value 0.17) (t = 21.043, P <0.01). Conclusion: HGF can reduce the range of myocardial infarction, reduce the rate of cardiomyocyte apoptosis and can inhibit left ventricular remodeling and improve cardiac function after myocardial infarction, and its mechanism may be related to its anti-apoptosis