补阳还五汤通过抑制p38有丝分裂原激活蛋白激酶通路改善大鼠缺血性脑损伤  

BuYangHuanWu recipe attenuates cerebral ischemia injury by inhibiting p38MAPK signal pathway in rats

作　　者：赵雅宁[1] 刘乐[1] 安朝旺[1] 李建民[1] 陈长香[1] 李淑杏[1] 

机构地区：[1]华北煤炭医学院康复医学系,唐山063000

出　　处：《解剖学杂志》2011年第1期48-51,共4页Chinese Journal of Anatomy

基　　金：河北省科技厅课题基金（2009276103D-3）

摘　　要：目的：探讨补阳还五汤针剂对缺血性脑卒中的治疗作用及机制.方法：大鼠分为假手术组,模型组,补阳还五汤高、低剂量组.参照Zea-Longa线栓法建立大鼠局灶性脑缺血模型.术后H-E染色观察海马区神经细胞形态变化,免疫组织化学法和免疫印迹法检测海马区磷酸化有丝分裂原激活蛋白激酶（p38MAPK）和环氧化酶-2（COX2）表达,原位缺口末端标记法（TUNEL）检测凋亡细胞.伤后3～7d水迷宫法测试动物学习记忆功能.结果：与对照组比较,脑缺血后海马区神经元结构损伤明显、磷酸化p38MAPK水平（术后1、6、24h）、COX2蛋白（术后1、6、24、48h）、凋亡神经细胞数量（6、24、48、72h）增加;大鼠的学习记忆功能下降;与模型组比较,补阳还五汤组中大鼠的学习记忆功能改善,神经元形态结构损伤减轻,磷酸化p38MAPK、COX2蛋白以及神经细胞凋亡数量下降,上述变化在高剂量补阳还五汤组更为明显.结论：补阳还五汤对脑缺血再灌注损伤有很好的治疗作用,其机制与调控p38MAPK/COX2信号通路,抑制神经细胞凋亡有关.Objective： To investigate the effects of BuYangHuanWu recipe on cerebral ischemia and its underlying mechanism in rats. Methods： Male SD rats were divided randomly into four groups： sham group, model group, low and high dose of BuYangHuanWu recipe treatment groups. Cerebral ischemia model was formed by middle cerebral artery occlusion （MCAO） with nylon suture according to the description of Zea-Longa＇s method. Morphological changes in the hippocampal region were observed by H-E staining; The expressions of p38MAPK phosphorylation and COX2 were detected by immunohisto- chemistry and Western-blot; The quantities of apoptotic ceils was measured with TUNEL method; Learning and memory function （Morris water maze） was performed daily from 3 d to 7 d after injury. Results： Compared with the sham group, some neurons in the model group displayed changes of necrosis and apoptosis; The p38MAPK phosphorylation （1,6,24 h post operation） and COX2 expressions （1,6,24,48 h post operation） and the number of neural apoptotic cells （6,24,48,72 h post operation） were enhanced; Learning and memory function was significantly decreased; latency to find the platform prolonged. Compared with the model group, the morphological damage of the brain tissues was obvious; the p38MAPK phosphorylation and COX2 expressions, and the number of neural apoptotic cells were decreased significantly; and latency to find the .platform was shorten. The above mentioned changes were more significant in the high-dose BuYangHuanWu recipe group. Conclusion： BuYangHuanWu recipe has good therapeutic effect on cerebral ischemia iniury and the molecular mecha- nism is related to attenuate p38MAPK/COX2 pathway and reduce neuronal apoptosis following MCAO.

关 键 词：补阳还五汤 脑缺血 有丝分裂原激活蛋白激酶 环氧化酶-2 

分 类 号：R365[医药卫生—病理学]