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目的:探讨血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)基因对缺血脑组织脑梗死神经细胞的保护作用与Bax和Bcl-2水平的关系,以及VEGF作用的机制。方法:用线拴法制成Wistar大鼠大脑中动脉永久性闭塞模型,将VEGF165真核表达质粒(pUCCAGGS/hVEGF165)经颅骨注入到缺血区。术后7d断头取脑,用反转录PCR(RT-PCR)检测VEGFmRNA的表达强度,用免疫组织化学方法检测Bax,Bcl-2和VEGF的表达水平。结果:与对照组相比,治疗组VEGFmRNA的表达增强,VEGF表达增高犤(32.50±2.45)个/高倍视野比(3.33±1.03)个/高倍视野,t=334.821,P<0.01犦,Bax表达减弱犤(4.11±0.41)个/高倍视野,t=9.168,P<0.01犦,Bcl-2表达增强犤(7.94±0.49)个/高倍视野,t=5.335,P<0.01犦。结论:VEGF165基因可以转化到缺血脑组织中并表达VEGFmRNA和VEGF,后者可能通过抑制Bax和增强Bcl-2的表达而保护神经细胞。
AIM: To investigate the relationship between the protective effect of vascular endothelial growth factor (VEGF) gene on cerebral infarction neurons and the expression of Bax and Bcl-2 in ischemic brain tissue and the mechanism of VEGF. Methods: The permanent occlusion model of middle cerebral artery in Wistar rats was made by tethering method. The VEGF165 eukaryotic expression plasmid (pUCCAGGS / hVEGF165) was injected into the ischemic area through the skull. The brain was decapitated 7 days after operation and the expression of VEGFmRNA was detected by RT-PCR. The expression of Bax, Bcl-2 and VEGF were detected by immunohistochemistry. Results: Compared with the control group, the expression of VEGFmRNA and the expression of VEGF in the treatment group increased (32.50 ± 2.45) / high power field ratio (3.33 ± 1.03) / high power field, t = 334.821, P <0.01 (4.11 ± 0.41) / high magnification field, t = 9.168, P <0.01 犦, and the expression of Bcl-2 increased 犤 (7.94 ± 0.49) / high power field, t = 5.335, P <0.01 犦. Conclusion: VEGF165 gene can be transformed into ischemic brain tissue and express VEGF mRNA and VEGF, which may protect nerve cells by inhibiting Bax and increasing Bcl-2 expression.