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探讨外源性神经生长因子(NGF)在大鼠心肌梗死后延迟再灌注治疗中的作用及机制。通过建立大鼠心梗延迟再灌注模型,构建重组腺病毒Ad-NGF基因并进行基因转染,使大鼠心梗延迟再灌注后体内NGF持续高表达。在术后第3、7、和/或14、28天检测NGF蛋白表达、微血管增生数量,观察心肌细胞凋亡情况、心脏结构及功能的变化。我们发现,给予NGF治疗的过表达组,NGF各时间点含量均高于对照组(P<0.01),凋亡率均低于模型对照组(P<0.01或P<0.05);过表达组新生微血管数量在第14天、28天明显高于模型对照组(P<0.01,P<0.05)。超声心动图记录第28天时模型对照组左室舒张/收缩末期内径测值明显高于过表达组(P<0.05),左室舒张/收缩末期容积测值明显高于过表达组(P<0.01),即模型对照组心脏结构改变明显;第14天和第28天时过表达组左室射血分数、短轴缩短率均明显高于模型对照组(P<0.01),即过表达组心功能较模型对照组明显改善。因此我们认为,外源性NGF通过促进血管增生和抑制心肌细胞凋亡等途径改善了大鼠心肌重塑及心脏功能。
To investigate the role and mechanism of exogenous nerve growth factor (NGF) in delayed reperfusion after myocardial infarction in rats. Through the establishment of delayed reperfusion model of myocardial infarction in rats, the recombinant adenovirus Ad-NGF gene was constructed and gene transfection was performed to prolong the expression of NGF in rats after delayed reperfusion. On the 3rd, 7th, and / or 14th and 28th day after surgery, the expression of NGF, the number of microvessel hyperplasia, the cardiomyocyte apoptosis and the changes of cardiac structure and function were observed. We found that the NGF-treated overexpression group had higher levels of NGF at each time point than those in the control group (P <0.01), and the apoptosis rates were lower than those in the model control group (P <0.01 or P <0.05) The number of microvessels was significantly higher on the 14th day and the 28th day than that of the model control group (P <0.01, P <0.05). Echocardiography recorded left ventricular end-diastolic / end-systolic diameter measured at day 28 in the model control group was significantly higher than the overexpression group (P <0.05), left ventricular diastolic / end systolic volume was significantly higher than the overexpression group (P <0.01 ), That is, the cardiac structure of the model control group changed significantly. On the 14th day and 28th day, the left ventricular ejection fraction and the short axis shortening rate in the overexpression group were significantly higher than those in the model control group (P <0.01) Compared with the model control group significantly improved. Therefore, we think that exogenous NGF can improve myocardial remodeling and cardiac function in rats by promoting vascular proliferation and inhibiting myocardial cell apoptosis.