bFGF对大鼠缺血性脑损伤CaMKⅡmRNA表达影响  

Effects of bFGF on the expression of CaMK Ⅱ mRNA in hippocampus and cortex after cerebral ischemia and reperfusion in rats

作　　者：邢雪松[1] 吕威力[1] 

机构地区：[1]沈阳医学院基础医学院解剖教研室,沈阳110034

出　　处：《中国公共卫生》2008年第7期810-812,共3页Chinese Journal of Public Health

基　　金：辽宁省教育厅科学研究计划项目(05L442)

摘　　要：目的研究大鼠脑缺血再灌注后Ca2+/钙调蛋白依赖的蛋白激酶Ⅱ(CaMKⅡ)mRNA的表达,探讨碱性成纤维细胞生长因子(bFGF)对脑组织缺血再灌注神经元CaMKⅡmRNA的调节作用及机制。方法应用线栓法制作大鼠局灶性脑缺血再灌注模型,大脑中动脉阻塞1 h再灌注损伤24 h,采用TUNEL法、逆转录聚合酶链反应(RT-PCR)检测海马及皮质内神经元凋亡和CaMKⅡmRNA的表达。结果大鼠缺血再灌注海马及顶叶皮质内神经元凋亡数增加,而CaMKⅡmRNA表达较假手术组减少,注射bFGF后神经元凋亡数减少,CaMKⅡmRNA表达明显高于缺血再灌注组。结论bFGF抑制缺血神经元凋亡,参与CaMKⅡmRNA的调节,对缺血神经元有保护作用。Objective To investigate the expression of CaMK Ⅱ mRNA in hippocarapus and cortex after cerebral ischemia reperfusion in rats, explore the regulative effects and the mechanism of basic fibroblast growth factor （bFGF） on CaMK Ⅱ mRNA in the brain tissue of the rats. Methods The model of middle cerebral artery occlusion（MCAO） was performed by using the intraluminal filament method. The expression of CaMK Ⅱ mRNA and neuron apoptosis in hippocampus and cortex were detected with RT - PCR TUNEL method. Results The expression of CaMK Ⅱ mRNA in hippocampus and cortex reduced after cerebral ischemia reperfusion. The expression of CaMK Ⅱ mRNA in bFGF group was increased, but neuron apoptosis decreased. Conclusion Basic fibroblast growth factor neuron inhibits apoptosis and participates in the regulation of expression of CaMK Ⅱ mRNA in ischemic neurons and protects the neurons.

关 键 词：脑缺血 BFGF CaMKⅡmRNA 海马 凋亡 

分 类 号：Q343[生物学—遗传学]