摘要
目的探讨转染bcl-2基因治疗大鼠局灶性脑缺血的作用机制是否与bFGF蛋白的表达增加有关。方法采用线栓法制作大鼠MCAO模型,取150只Wistar大鼠,随机分成三组,分别为脑室内注射生理盐水组(生理盐水组)、脑室内注射空质粒组(空质粒组)和脑室内注射质粒pLXSN介导的bcl-2基因组(Bcl-2组)。每组50只。分别在缺血再灌注后3、6、24、48、72h观察bFGF蛋白表达的变化。结果大鼠MCAO后bFGF蛋白在生理盐水组与空质粒组之间,缺血后各个时间点的表达均无显著性差异(P>0.05),结果显示其表达高峰在缺血后24h,而bcl-2组早期即大量表达且持续较长时间,并在同一时间段表达明显强于其他组(P<0.05)。结论pLXSN-bcl-2基因脑保护机制可能是通过促进bFGF的表达而实现的。
Objective To study the protective effct of bcl-2 against neuroal injury and the possible roles of alteration in the expression of bFGF following cerebral ischemia in rat. Methods 150 wistar rats were randomly assingned in 3 groups （bc1-2 treated group,saline group and pLXSN group）,there were 50 rats in each group. And we studied the bFGF expression in 3,6,24,48,72hours after MCAO temporary ischemia of the MCAO for 2 hours was induced, Results The expression of bFGF in the saline group and pLXSN group weren＇t different in each time（P〉 0.05）, bFGF expressed early in the bcl-2 group and lasted for a long time,while its expression was more than other groups at the same time. Conclusion Bcl-2 can effectivly attenuate ischemic brain injury and increase the expression of bFGF in the ischemic brain, indicating that the neuroprotective of estrogen is associated with up-regulation of bFGF in cerebral ischemia.
出处
《中国现代医生》
2009年第13期34-35,共2页
China Modern Doctor
