FKBP51在全脑缺血再灌注损伤中的作用  

Effects of FKBP51 on Global Cerebral Ischemia/Reperfusion Injury

作　　者：王凯[1] 张风玉[1] 魏秀娥[2] 荣良群[2] 

机构地区：[1]徐州医学院研究生学院,江苏徐州221002 [2]徐州医学院第二附属医院,江苏徐州221002

出　　处：《北华大学学报（自然科学版）》2013年第2期168-171,共4页Journal of Beihua University（Natural Science）

基　　金：徐州市科技计划发展项目(XF10C030;2010)

摘　　要：目的探讨FKBP51在全脑缺血再灌注损伤中的作用机制.方法采用四血管动脉阻塞(4-V0)大鼠全脑缺血模型,应用免疫印迹进行分析,将实验大鼠随机分成假手术组(Sham组)、缺血/复灌组(Ir组)、溶剂对照组(TE buffer组)和给药组(FKBP51的反义寡核苷酸AS.ODN组及MS.ODN组).结果 FKBP51在大鼠脑组织中有所表达,下调FKBP51表达后促细胞存活蛋白Akt磷酸化增强.结论 FKBP51参与了脑缺血损伤,同时参与了抑制PKB/Akt信号通路,从而导致脑缺血复灌后神经元的损伤.FKBP51是脑缺血再灌注损伤过程中抑制神经元存活的机制之一.Objective To explore the action mechanism of FKBPS1 in the global cerebral ischemia/reperfusion injury. Method Pulsinelli-Brierley four-vessel occlusion method was used to establish a global cerebral ischemia model and western blot was applied for the analysis. The rats were randomly divided into sham group, ischemia/ reperfusion group, solvent control group and treatment group. Results FKBP51 was expressed in the cerebral tissue of the rats to some extent and down-regulating the FKBP51 expression could promote the phosphorylation of surviving Akt. Conclusion FKBP51 may be involved in the cerebral ischemia injury and also in the inhibition of PKB/Akt signal pathway that leads to the neuronal damage induced by cerebral ischemia/reperfusion, which may be one of mechanisms through which the neuron survival can be inhibited in the process of cerebral ischemia/ reperfusion injury.

关 键 词：FKBP51 PHLPP AKT 反义寡核苷酸 

分 类 号：R741[医药卫生—神经病学与精神病学]