中文摘要：

目的：本文旨在观察间歇性低压低氧（珊）预处理诱导脑缺血耐受过程中，大鼠海马CA1区磷酸化p38MAPK（p-p38MAPK）的表达以及表达p-p38MAPK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）0nfin组、m＋8hanl0min组、shanl7d组、IH＋snam 7d组、损伤性缺血（Is）7d组、IH＋Is7d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p-p38MAPK的表达；免疫荧光双标法观察表达p-p38MAPK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-p38MAPK的表达明显增加，且上调星形胶质细胞中p-p38MAPK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-re8MAPK上调可能是IH预处理保护脑的一个途经。

英文摘要：

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.