脑缺血预处理对沙鼠脑缺血再灌注损伤 p38MAPK活化的作用

目的 探讨脑缺血预处理对脑缺血后p38MAPK信号的影响.方法 蒙古沙鼠分成对照组、脑缺血再灌注组、脑缺血预处理组和抑制剂SB203580组.制备脑缺血及脑缺血预处理动物模型.免疫组织化学法和蛋白质印迹法检测海马区磷酸化p38MAPK的表达,TUNEL 法检测神经细胞凋亡,TTC染色测定脑梗死体积.结果 与对照组比较,脑缺血再灌注组磷酸化p38MAPK表达增高,凋亡神经细胞数量增加(P<0.05),磷酸化p38MAPK阳性细胞与TUNEL阳性细胞为同一神经元.与脑缺血再灌注组比较,脑缺血预处理组凋亡神经细胞下降、磷酸化p38MAPK表达较少、梗死面积缩小(P<0.05);抑制剂SB203580组磷酸化p38MAPK表达水平与脑缺血预处理组相似,但两组神经细胞凋亡数量及脑梗死体积比较,差异有统计学意义(P<0.05).结论 缺血预处理对脑缺血性损伤具有保护作用,其机制并非完全依赖p38MAPK信号活化.

Abstract：

Objective To study the effect of ischemic preconditioning on p38MAPK pathway after ischemia - reperfusion injury in gerbils. Method Gerbils were divided randomly into control group, ischemia - reperfusion group ( I/R ) , ischemia preconditioning group ( IP ) and inhibitor SB203580 group. Transient ischemia - reperfusion model and ischemia preconditioning model were performed. The expression levels of p38MAPK phosphorylation were detected by immunohistochemistry and Western blot, the neurons apoptosis were detected by TUNEL method and the infarction volume assessments were performed by TTC staining. Results Compared with control group, there were higher expression levels of p38MAPK phosphorylation,more apoptotic neurons in I/R group. The p38MAPK phosphorylation \positive cells and TUNEL positive cells were located in the same neurons. Compared with I/R group, there were lower expression levels of p38MAPK phosphorylation,fewer apoptotic neurons and smaller infarction volumes in IP group( P <0.05). The levels of p38MAPK phosphorylation in SB203580 group were similar as those in IP group( P > 0. 05 ) . However, the number of apoptotic neurons and infarction volumes were obviously changed ( P <0.05). Conclusions IP has protective effect from I/R damage in gerbils, which might be not only involved p38MAPK pathway.

Effect of ischemic preconditioning on p38MAPK activation after cerebral ischemia-reperfusion in gerbil

Objective To study the effect of ischemic preconditioning on p38MAPK pathway after ischemia - reperfusion injury in gerbils. Method Gerbils were divided randomly into control group, ischemia - reperfusion group ( I/R ) , ischemia preconditioning group ( IP ) and inhibitor SB203580 group. Transient ischemia - reperfusion model and ischemia preconditioning model were performed. The expression levels of p38MAPK phosphorylation were detected by immunohistochemistry and Western blot, the neurons apoptosis were detected by TUNEL method and the infarction volume assessments were performed by TTC staining. Results Compared with control group, there were higher expression levels of p38MAPK phosphorylation,more apoptotic neurons in I/R group. The p38MAPK phosphorylation \positive cells and TUNEL positive cells were located in the same neurons. Compared with I/R group, there were lower expression levels of p38MAPK phosphorylation,fewer apoptotic neurons and smaller infarction volumes in IP group( P <0.05). The levels of p38MAPK phosphorylation in SB203580 group were similar as those in IP group( P > 0. 05 ) . However, the number of apoptotic neurons and infarction volumes were obviously changed ( P <0.05). Conclusions IP has protective effect from I/R damage in gerbils, which might be not only involved p38MAPK pathway.