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间歇性低压低氧预处理对脑缺血大鼠海马p-p38 MAPK表达的影响
引用本文:毕新颖,王天爽,张敏,刘青青,李文斌,张翼. 间歇性低压低氧预处理对脑缺血大鼠海马p-p38 MAPK表达的影响[J]. 中国应用生理学杂志, 2014, 0(2): 97-100,I0001,I0002
作者姓名:毕新颖  王天爽  张敏  刘青青  李文斌  张翼
作者单位:[1]河北医科大学病理生理学教研室,石家庄050017 [2]河北省脑老化与认知神经学实验室,石家庄050031 [3]河北医科大学生理学教研室,石家庄050017
基金项目:国家自然科学基金资助项目(31271149,81271454);2013年地方高校国家级大学生创新创业训练计划项目(201310089005);2013年河北省大学生创新创业训练计划(201310089005).
摘    要:目的:本文旨在观察间歇性低压低氧(IH)预处理诱导脑缺血耐受过程中,大鼠海马CA1区磷酸化p38MAPK(p-p38 MAPK)的表达以及表达p-p38 MAPK的星形胶质细胞数量。方法:将30只健康雄性Wistar大鼠随机分为6组(n=5):假手术(sham)0 min组、IH+sham 0 min组、sham 7 d组、IH+sham 7 d组、损伤性缺血(Is)7 d组、IH+Is 7 d组。通过硫堇染色对各组大鼠海马CA1区锥体神经元进行神经病理学评价;免疫组织化学染色观察pp38 MAPK的表达;免疫荧光双标法观察表达p-p38 MAPK的星形胶质细胞数量。结果:IH预处理可以诱导脑缺血耐受,同时引起大鼠海马CA1区p-p38 MAPK的表达明显增加,且上调星形胶质细胞中p-p38 MAPK的表达。结论:低压低氧预处理促大鼠海马CA1区锥体神经元和星形胶质细胞中p-p38MAPK上调可能是IH预处理保护脑的一个途经。

关 键 词:IH预处理  脑缺血耐受  p-p38  MAPK  免疫组织化学  免疫荧光  海马CAI区  星形胶质细胞

The up-regulation of p-p38 MAPK during the induction of brain ischemic tolerance induced by intermittent hypobaric hypoxia preconditioning in rats
BI Xin-ying,WANG Tian-shuang,ZHANG Min,LIU Qing-qing,LI Wen-bin,ZHANG Yi. The up-regulation of p-p38 MAPK during the induction of brain ischemic tolerance induced by intermittent hypobaric hypoxia preconditioning in rats[J]. Chinese journal of applied physiology, 2014, 0(2): 97-100,I0001,I0002
Authors:BI Xin-ying  WANG Tian-shuang  ZHANG Min  LIU Qing-qing  LI Wen-bin  ZHANG Yi
Affiliation:1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017; 2. Aging and Cognition Neuroscience Laboratory of Hebei Province, Shijiazhuang, 050031; 3. Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China)
Abstract:Objective: To explore the expression of p-p38 MAPK protein and the number of astrocytes expressing p-p38 MAPK in CA1 hippocampus in rats during the induction of brain ischemic tolerance induced by intermittent hypobaric hypoxia (IH) preconditioning. Metla otis: Thirty healthy adult male Wistar rats were randomly divided into 6 groups ( n = 5 in each group) : sham 0 rain group, IH + sham 0 rain group, sham 7 d group, IH + sham 7 d group, Ischemia (Is) 7 d group, and IH + Is 7 d group. Neuropathological evaluation was per formed by thionine staining in CA1 hippocampus in rats. The expression of p-p38 MAPK in CA1 hippocampus was observed by immunohisto chemical staining. And the nttmber of astrocytes expressing p-p38 MAPK was observed by immunofluorescent double labeling. Results: The results showed that IH preconditioning induced brain ischemic tolerance successfully. At the same time, IH preconditioning obviously up-regu lated the expression of p-p38 MAPK protein in CA1 hippocampus, and also increased the number of astrocytes expressing p-p38 MAPK. Con clusion: It might be concluded that IH preconditioning induced brain ischemic tolerance by up-regulating the expression of p-p38 MAPK protein in pyramidal neurones and astrocytes.
Keywords:intermittent hypobaric hypoxia preconditioning  brain ischemic tolerance  p-p38 MAPK  immtmohistochemistry  immunofluorescent  hipix~ampal CA1 region  astrocytes
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