血管内皮生长因子_(165)对局灶性脑梗死的影响

Vascular endothelial growth factor_(165) can reduce the cerebral lesion caused by focal cerebral ischemia in rats

目的 探讨血管内皮生长因子16 5 (VEGF16 5 )基因对大鼠脑梗死的治疗作用。方法 用线栓法制成Wistar大鼠持续性大脑中动脉闭塞 (MCAO )模型 ,将质粒载体与VEGF16 5 基因构成的重组DNA(puCCAGGS/hVEGF16 5 )经颅骨孔注入到梗死区。术后第 8天断头取脑 ,经 2 %红四氮唑染色后测定各组脑梗死体积 ,采用逆转录PCR和免疫组织化学方法检测VEGF16 5 基因的表达及血管增生情况。结果 治疗组VEGFmRNA、VEGF蛋白表达高 ,治疗组脑梗死区周围血管数量为 50 .76条 /高倍镜视野 (× 40 0 ) ,明显高于对照组的 40 .67条 /高倍镜视野 (× 40 0 ) ,P <0 .0 1;治疗组脑梗死体积为 9.3 2 % ,明显小于对照组的 2 3 .68% ,P <0 .0 1。结论 在质粒载体的介导下 ,VEGF16 5 基因可以转化到缺血脑组织中 ,并表达VEGF16 5 蛋白 ,可明显缩小脑梗死体积 。

Objective To study the effects of naked DN A encoding vascular endothelial growth factor 165 (VEGF 165 )on cerebra l infarction in rats. Methods Following establishme nt of a permanent middle cerebral artery occlusion (MACO) model by nylon suture embolization in Wistar rats, the puCCAGGS/hVEGF 165 was directly injected i nto the ischemic tissues through skull hole. Seven days later, the rats were sac rificed. The infarct volume was measured by 2% TTC staining technique, then the expression of VEGF 165 gene and vascular proliferation were measured by use of RT-PCR and immumohistochemistry methods. Results Expression of VEGF 165 mRNA and VEGF protein in the therapy group increas ed. Compared with the control group, the number of vessels of the therapy group was significantly higher (50.76/HPF vs 40.67/HPF)( P <0.01), and the infarct v olume of therapy group was obviously smaller in the therapy group (9.32% vs 23.6 8%) ( P <0.01). Conclusion Topically applied VEGF 165 gene can be transformed into the ischemia tissues in the brain and expre ss VEGF 165 protein, which can help promote vascular proliferation and redu ce the infarct volume.