大鼠正常血糖脑缺血及高血糖脑缺血时p38MAPK的表达

Expression of p38 Mitogen-activated Protein Kinase on Cerebral Ischemia Under Hyperglycemia

目的探讨p38MAPK与脑缺血及高血糖脑缺血损害的关系。方法实验大鼠随机分为3组:(1)高血糖脑缺血组(简称高血糖组,20只),于脑缺血术前30min尾静脉注射25%葡萄糖(4g/kg);(2)正常血糖脑缺血组(简称正常血糖组,20只),于脑缺血术前30min尾静脉注射等量18%D-甘露醇;(3)手术非缺血性对照组(10只)。采用双侧颈动脉结扎和放血法在高血糖组和正常血糖组制造全脑缺血模型,通过免疫组织化学技术与Western blot免疫印迹技术对比检测缺血30min,再灌注1、3、6h各时间点脑组织p38MAPK表达。结果对照组海马CAI区、CAIII区,未见p38MAPK阳性神经元;免疫组化在CAI区和CAIII区,在缺血30min,再灌注13、、6 h不同时间点高血糖组阳性细胞数与正常血糖组比较差异无统计学意义(P>0.05);Western blot检测可见正常血糖组和高血糖组脑缺血30min,再灌注1、36、h时激活的p38MAPK蛋白明显增加,高血糖组灰度比值(分别为7.25±1.91、8.64±2.41、9.58±2.98、12.00±3.01)与正常血糖组(分别为6.68±1.51、7.92±1.75、8.34±2.00、9.02±2.27)比较,p38MAPK差异无统计学意义(P>0.05)。结论脑缺血再灌注时p38MAPK被激活,参与缺血性损伤的发生,但高血糖并不能明显增加p38MAPK的总量,故在高血糖加重脑缺血性损伤中p38MAPK可能不发挥主要作用。

Objective To explore the relationship between expression of p38MAPK and cerebral ischernia exacerbated by hyperglycemia. Methods Transient cerebral ischemia for 30 rain duration was induced by bilateral clamping of the carotid arterial and withdrawing blood dropped blood in rats. p38MAPK in the brain were contrastively examined by means of immunohistological and Western blot techniques following global cerebral ischemia in rats with and without hyperglycemia. Results In CAⅠ and CAⅢ of hippocampal, The number of im munohistochemistry-positive cell in hyperglycemic group was significantly higher than that in control group, but there was no significant difference in the number of immunohistochemistry-positive cells between hyperglycemic group and normoglycemic group at the same time point. There was no significant difference in the activation of p38MAPK between normoglycemic group and hyperglycemic group by Westem blot. Conclusions The activation of p38MAPK can occur in the process of cerebral ischemia/reperfusion and the amount of phospho-p38 was not altered by ischemia under both normo-and hyperglycemic conditions.