氯化锂在肢体缺血后处理中对脑缺血再灌注大鼠的糖原合酶激酶3β/微管相关蛋白2a/b通路的影响  

Effects of lithium chloride in the limb ischemia postconditioning on glycogen synthase kinase 3β/microtubule associated protein 2a/b pathway of cerebral ischemia reperfusion rats

作　　者：刘芳怡[1] 刘开祥[1] 李浩[1] 廖小明[1] 吴岚[1] 齐立[1] 唐永刚[1] 

机构地区：[1]桂林医学院附属医院神经内科,541000

出　　处：《临床神经病学杂志》2014年第6期442-445,共4页Journal of Clinical Neurology

基　　金：广西自然科学基金(2012GXNSFAA053102);桂林市科技局第一批科学研究与技术开发项目(20110119-1-6)

摘　　要：目的探讨肢体缺血后处理中氯化锂对脑缺血再灌注大鼠糖原合酶激酶3β(GSK3β)及其下游微管相关蛋白2a/b(MAP2a/b)的影响。方法将60只雄性SD大鼠随机分为假手术组,缺血再灌注组(I/R组),肢体缺血后处理组(Lpost C组)和氯化锂组(Li Cl组),15只每组。制作脑缺血再灌注,肢体缺血后处理及氯化锂干预大鼠模型,于大鼠脑缺血再灌注24 h后进行神经功能缺损评分和大鼠脑梗死体积测定;应用Western blotting法检测P-GSK3β(ser9),MAP2a/b的蛋白表达。结果除了假手术组,I/R组神经功能缺损评分和脑梗死体积最大,Lpost C组较小,Li Cl组神经功能缺损评分和脑梗死体积最小(均P<0.05)。与I/R组相比,Lpost C组磷酸化GSK3β(P-GSK3β)(ser9)及MAP2a/b表达增高(均P<0.05)。与Lpost C组相比,Li Cl组P-GSK3β(ser9)及MAP2a/b表达明显升高(均P<0.05)。结论肢体缺血后处理使P-GSK3β(ser9)表达增加,激活GSK3β/MAP2a/b信号通路对脑缺血再灌注损伤起保护作用。氯化锂通过增加MAP2 a/b的稳定性增强对脑缺血后处理的脑保护作用。Objective To study the effects of lithium chloride in the limb ischemia postconditioning on glycogen synthase kinase 3β（ GSK313） and the its downstream microtubule associated protein 2a/b （MAP2a/b） in rats with cerebral ischemia reperfusion . Methods Sixty male SD rats were divided into sham operation group, cerebral ischemia reperfusion group（ I/R group）, limb ischemia postconditioning group （LpostC group ） and lithium chloride group （LiC1 group）, 15 rats in each group. Cerebral ischemia reperfusion, limb ischemia postconditioning and lithium chloride intervention model were made, neurological function deficit score and infarct volume determination were conducted 24 h after cerebral ischemia reperfusion injury. The protein expression of P-GSK3β, MAP2a/b were tested by Western blotting. Results Excepted sham operation group, nerve function defect score and cerebral infarction volume in I/R group were the biggest, in LpostC group were smaller, in LiC1 group were the smallest（ all P 〈0.05 ）. Compared with I/R group, phosphoralation of GSK313 （P-GSK3β） （set9） and MAP2a/b in LpostC group had increased（ all P 〈 0.05 ）. Compared with LpostC group, P-GSK3 β （serg） and MAP2a/b in LiC1 group had increase （ all P 〈 0.05 ）. Conclusions Limb ischemia postconditioning can increase P-GSK3β （ ser9 ） expression, activate GSK3β/MAP2a/b signaling pathway to protect the ischemia reperfusion injury. Lithium chloride can be used to increase the stability of MAP2a/b to enhance the brain nerve protective effect of ischemic postconditioning.

关 键 词：肢体缺血后处理 糖原合酶激酶3Β 微管相关蛋白2 a/b 氯化锂 

分 类 号：R743.3[医药卫生—神经病学与精神病学]