摘要
目的研究大鼠短暂大脑中动脉闭塞(MCAO)模型经侧脑室注射质粒pLXSN介导bcl-2基因后,该基因对脑梗死及脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的影响。方法取135只Wist-ar大鼠随机分配为3组,每组45只,对照组为脑室注射生理盐水和空质粒两组,治疗组为脑室注射Bcl-质粒pLXSN介导bcl-2基因。以改良线栓法制备短暂缺血2 h脑梗死模型,每组分别于缺血后3、6、24、48、72 h为时间点。分别测量梗死体积变化以及BDNF蛋白的表达。结果MCAO后24、487、2 h,梗死体积治疗组显著小于对照组(P<0.05);36、h时间点无显著变化(P>0.05)。MCAO后24、487、2 h,治疗组Bcl-2和BDNF蛋白的表达较对照组显著增加(P<0.01),而3、6 h时间点无显著改变(P>0.05)。结论脑室注射质粒pLXSN介导bcl-2基因对短暂脑缺血有治疗作用,并可增加BDNF表达。上调BDNF表达所起的神经保护作用可能是短暂脑缺血后bcl-2基因的治疗作用机制之一。
Objective To study whether bcl-2 gcne can improve cerebral infarct and expression of brain-derived neurotrophic factor （BDNF） by intraventricular injection after temporarily middle cerebral artery occlusion （MCAO） in rat. Methods 135 wistar rat were randomly assigned in 3 groups （bcl-2-gene treated group, saline group and pLSXN group ）, there were 45 rats in every group. And we studied the infarct volumes and BDNF expression in 3, 6, 24, 48 and 72 h after MCAO. Temporary ischemia of the MCA for 2 h was induced by the suture occlusion technique. 20μL plasmid pLXSN-mediated transfer bcl-2 gene was injected intraventricularly after MCAO was established. Results The infarction volume of the treaty group are significantly less than the control group in 24, 48, 72 h after MCAO （P〈0. 05）. However, there aren＇t different between three groups in 3 and 6 h after MCAO （P〉0.05）. The expression of Bcl-2 and B1）NF are significantly increased in treated group in 24,48 and 72 h after MCAO （P〈0. 01）; In 3,6 h after MCAO, the expression of Bcl-2 and BDNF are same between treated group and control group （P〉0.05）. Conclusions Our study demonstrated bcl-2 gene can decrease cerebral infarct size and increase expression of BDNF by intraventricular injection. One possible mecha- nism of action of bcl-2 gcne after temporary iscbcmia appears to be the ncuroprotection of up-regulated BDNF.
出处
《中国神经免疫学和神经病学杂志》
CAS
2005年第6期331-334,共4页
Chinese Journal of Neuroimmunology and Neurology
基金
辽宁省自然科学基金资助项目(20032054)
