NGF预处理对AMI大鼠心肌VEGF及其受体KDR/flk-1表达的影响

目的研究神经生长因子（NGF）预处理对急性心肌梗死（AMI）大鼠心肌中VEGF及其受体KDR/flk-1表达的影响。方法雄性成年Wistar大鼠60只,随机分为3组：NGF预处理组和非NGF预处理组和对照组（每组20只）。大鼠NGF预处理使用注射用鼠神经生长因子（0.5μg/kg）尾静脉注射。采用电凝烧灼左冠状动脉前降支制作大鼠急性心肌梗死动物模型。观察各组大鼠心肌损伤的病理改变;以RT-PCR方法检测大鼠心肌组织中血管内皮生长因子（VEGF）及其受体KDR/flk-1的表达情况。结果大鼠心肌坏死面积组间比较差异有统计学意义（F=12.13,P〈0.01）,NGF预处理组（25.41±9.06）%明显少于非NGF组（40.08±11.38）%,P〈0.01。大鼠心肌VEGF、KDR/flk-1mRNA表达组间比较差异有统计学意义（F=18.23,14.10,P均〈0.01）;NGF预处理组VEGF（45.41±11.54）、KDR/flk-1（47.40±7.83）均高于非NGF组VEGF（32.34±8.10）、KDR/flk-1（31.09±7.88）,P均〈0.01。大鼠心肌VEGF mRNA表达与其受体KDR/flk-1 mRNA表达呈正相关关系（r=0.691,P〈0.01）。结论 NGF预处理可能通过上调VEGF及其受体表达,增加大鼠心肌中新生血管密度,减轻AMI大鼠心肌损伤。

Influence of Nerve Growth Factor Pretreatment on expression VEGF and KDR/flk -1 in AMI rats

Objective To investigate the effects of NGF（Nerve Growth Factor） pretreatment on expression VEGF and KDR/flk-1 of acute myocardial infaction in rats.Methods 60 male adult Wistar rats were randomly classified into three groups： the control（n=20）,non-NGF（n=20） and NGF（n=20） groups.The NGF group was injected NGF（0.5 μg/kg） via caudal vena.Then we performed left anterior descending coronary artery（LAD） ligation by means of electrotome.In this study we observe the morphologic changes of myocardial pathology in each group;To measure the expression of vascular endothelial growth factor（VEGF） and KDR/flk1 we use immunohistology and RT-PCR.Results Infarct areas of rats had statistically significant differences among groups（F=12.13,P0.01）,but the damage in NGF group（25.41±9.06）% was significantly less than non-NGF group（40.08±11.38）%,P0.01.Differences of VEGF,KDR/flk-1 mRNA expression had statistics significance between groups（F=18.23,14.10,all P0.01）.Compared to non-NGF group VEGF（32.34±8.10）、KDR/flk-1（31.09±7.88） were higher in the NGF group VEGF（45.41±11.54）、KDR/flk-1（47.40±7.83）,all P0.01.A positive correlation was showed between VEGF mRNA and KDR/flk-1 mRNA（r=0.691,P0.01）.Conclusion The NGF pretreaement can enhance the new vessels density in cardiac muscle,through the rise of expression of VEGF and KDR/flk-1,and lessen the myocardial damage induced by AMI in rats.