摘要
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 explore the protective effect of vascular endothelial growth factor(VEGF) on nerve cells after cerebral infarction(CI), and its relation with the expressions of Bax and Bcl 2,and study the mechanism of VEGF. METHODS:After establishment of a rat model of permanent middle cerebral artery occlusion(MCAO) by nylon suture embolization,the eukaryon expressed focal plasmid(pUCCAGGS/hVEGF165) was directly injected into the ischemic area via skull.After 7 days the rats were killed for brain, RT PCR was used to measure the expression of VEGF mRNA,and immunohistochemistry was used to measure the expression of VEGF,Bax and Bcl 2. RESULTS:Compared with the control group,the expression of VEGF mRNA was increased,the expression of VEGF was increased[(32.50±2.45) vs(3.33±1.03) per high power sight,t=334.821,P< 0.01],the expression of Bax was weakened[(4.11±0.41) per high power sight,t=9.168,P < 0.01], and the expression of Bcl 2 was strengthened[(7.94±0.49) per high power sight,t=5.335,P< 0.01]. CONCLUSION:VEGF165 gene can transform into the ischemic brain tissue and express VEGF mRNA and VEGF,and VEGF protein protects nerve cells by restraining the expression of Bax and impelling the expression of Bcl 2.
出处
《中国临床康复》
CSCD
2004年第28期6063-6065,共3页
Chinese Journal of Clinical Rehabilitation