脑源性神经营养因子在预缺血模型神经保护中的作用  

The neuroprotective role of BDNF in ischemic preconditioning model

作　　者：许静[1] 齐素华[2] 张光毅[2] 

机构地区：[1]徐州医学院机能学实验中心,江苏徐州221002 [2]徐州医学院生物化学与分子生物学研究中心

出　　处：《徐州医学院学报》2010年第4期227-229,共3页Acta Academiae Medicinae Xuzhou

基　　金：国家自然科学基金重点项目(90608015);江苏省教育厅基金(08KJB180010)

摘　　要：目的研究脑源性神经营养因子(BDNF)在预缺血模型中的表达水平及作用,以探讨缺血耐受形成的分子信号机制。方法制备SD大鼠大脑四动脉结扎模型及预缺血模型,采用免疫印迹、免疫沉淀等技术,检测各实验组中BDNF表达、其受体酪氨酸激酶受体B(TrkB)和下游蛋白胞外信号调节蛋白激酶(ERK1/2)磷酸化的水平变化。结果预缺血组BDNF的表达、TrkB和ERK1/2磷酸化水平较缺血/再灌注组升高(P<0.05),而TrkB受体的拮抗剂K252 a可以降低其升高的激活水平(P<0.05)。结论预缺血激活BDNF-TrkB-ERK1/2信号通路实现其神经保护作用。Objective To investigate the expression level and the role of brain-derived neurotrophic factor（BDNF） in ischemic preconditioning（IP） model and the underlying molecular signaling mechanism of ischemic tolerance.Methods Ischemic preconditioning model was induced by the four-vessel occlusion in Sprague-Dawley rats.Immunoblotting and immunoprecipitation methods were employed to determine the variations in the expression level of BDNF,the phosphorylation levels of its receptor,tyrosine kinase receptor B（TrkB） and the downstream extracellular-signal-regulated kinase（ERK1/2）.Results In the IP group,the levels of BDNF expression and TrkB and ERK1/2 phosphorylation increased（P0.05）,as compared to the Ischemia/Reperfusion group,while the pretreatment with K252a,a TrkB receptor antagonist,reversed the preconditioning-induced increase in TrkB and ERK1/2 activation（P0.05）.Conclusion Ischemic preconditioning exerts the neuroprotective effect via the activation of BDNF-TrkB-ERK1/2 pathway.

关 键 词：脑源性神经营养因子 预缺血 缺血耐受 

分 类 号：R743.31[医药卫生—神经病学与精神病学]