姜黄素抗脑缺血再灌注损伤作用与MAPK信号通路的相关性分析

目的探讨姜黄素对大鼠脑缺血再灌注损伤中细胞外信号调节蛋白激酶（ERK1/2）、C-Jun氨基末端（JNK）/应激化蛋白激酶（SAPK）及p38MAPK信号转导通路的影响。方法采用线栓法阻塞大鼠大脑中动脉（MCAO）建立局灶性脑缺血模型,观察不同浓度姜黄素（20 mg/kg、40 mg/kg、80 mg/kg）对脑缺血再灌注损伤后大鼠神经行为学评分的影响,并用Western blot法检测p38MAPK、p-p38MAPK、ERK1/2、p-ERK1/2及JNK的表达。结果假手术组无神经行为学改变;各用药组神经行为学评分明显低于缺血再灌注组（P〈0.05）。与缺血再灌注组相比各用药组p-p38MAPK及JNK表达明显降低（P〈0.05）,而p-ERK1/2表达显著增加（P〈0.05）,p38MAPK及ERK1/2表达各组间差异无统计学意义（P〉0.05）。结论姜黄素对大鼠脑缺血再灌注损伤具有保护作用,其保护作用机制可能与抑制p38MAPK和JNK/SAPK信号转导通路以及增强ERK1/2信号转导通路有关。

Relationship between Protective Effect of Curcumin on Focal Cerebral Ischemia Reperfusion Injury and MAPK Signal Transduction System

Objective To investigate the effect of curcumin on expression of extracellular signal-regulated kinase（ERK）1/2,c-Jun NH2-terminal kinase（JNK）/stress activated protein kinase（SAPK）and p38 mitogen-activated protein kinase（MAPK）protein after focal cerebral ischemia reperfusion injury in rats.Methods The rat models with middle cerebral artery occlusion/reperfusion were established by thread-occluded method.The neurological deficiency scores were collected.The expression of p38MAPK,p-p38MAPK,ERK1/2,p-ERK1/2 and JNK protein after focal cerebral ischemia reperfusion injury in rats with curcumin in different concentration（20 mg/kg,40 mg/kg,and 80 mg/kg） were detected by Western blot.Results There was no neurological deficiency in sham-operated group.Compared with ischemia/reperfusion group,the neurological deficiency scores were obviously decreased in curcumin treatment group（P0.05）.The expression of p-p38MAPK and JNK protein were obviously improved（P0.05）.There was no significant difference of the expression of p38MAPK and ERK1/2 protein.Conclusion Curcumin had a protective effect on cerebral ischemia reperfusion injury in rats by inhibiting the function of p38MAPK and JNK signal transduction system and improving the function of ERK1/2 signal transduction system.