p38 MAPK在局灶性脑缺血大鼠缺血中心区和半影区的表达

Expression of p38 MAPK in cerebral ischemia core and penumbra in rats with focal cerebral ischemia

目的研究大鼠局灶性脑缺血不同缺血时间皮质半暗带和中心区p38丝裂原激活蛋白激酶(p38 MAPK)磷酸化水平和蛋白水平的表达。方法用线栓法建立大鼠局灶性脑缺血模型,分别于术后1、3、6、12、24 h剥取缺血半暗带及中心区皮质组织,应用Western blot并结合Gel Doc凝胶成像系统,定量检测p38 MAPK磷酸化水平和蛋白表达量。结果与假手术组相比,模型组大鼠皮层缺血核心区和半影区p38 MAPK磷酸化水平显著升高(P<0.05,n=6),缺血中心区p38 MAPK在缺血6 h磷酸化程度达高峰,半暗带在3 h时达高峰;各组间p38 MAPK蛋白表达量水平无明显变化。结论p38 MAPK磷酸化激活参与了大鼠脑缺血损伤过程的信号转导,在缺血中心区和半影区的磷酸化增强可能与局部脑缺血损伤的神经元坏死和凋亡过程有密切关系。

Objective To investigate the expression of phosphorylated p38 mitogen activated protein kinase （p-p38 MAPK ） and protein expression levels at different ischemic time point in focal cerebral ischemic core and penumbra of rats. Methods Focal ischemic models of middle cerebral artery occlusion （ MCAO ） in rats were made by inserting nylon thread. Brain samples were harvested from ischemic core and penumbra. Western blot combined with Gel Doc imagine systems were applied to examine the changes in p^p38 MAPK and protein expression levels in the brain of rats. Results Western blot results showed that phosphorylation levels of p38MAPK in the ischemic core and penumbra increased significantly at every ischemic time point when compared with sham group （P 〈 0. 05 ,n = 6 for each group ）. p-p38 MAPK peaked at 6 hours in core ischemia and at 3 hours in penumbra. However, there were no significant changes in p38 MAPK protein expression levels. Conclusion The activiated p38 MAPK may be involved in the signal transduction pathway of cerebral ischemia. The increase of p-p38 MAPK in the central area of ischemia and penumbra may play a role in neuronal necrosis and apoptosis.