摘要
目的探讨尤瑞克林对局灶性脑缺血再灌注损伤大鼠模型的神经保护作用及其可能的机制。方法 60只SD大鼠随机分为3组:假手术组、缺血再灌注损伤模型组和尤瑞克林治疗组,用线栓法制作大鼠大脑中动脉脑缺血再灌注损伤模型,缺血2 h再灌注24 h后,观察各组大鼠神经行为学评分,HE染色观察神经细胞组织形态变化,免疫组化法检测磷酸化p38MAPK的表达,TUNEL法检测凋亡细胞。结果与假手术组比较,模型组大鼠神经行为学评分明显升高(P<0.01),HE染色神经细胞受损明显(P<0.01),脑组织磷酸化p38MAPK表达水平、凋亡神经细胞数量明显增加(P<0.01)。与模型组比较,尤瑞克林治疗组大鼠的神经功能缺损得到改善、神经元形态结构损伤减轻、磷酸化p38MAPK表达水平以及神经细胞凋亡数量回降(P<0.01)。结论尤瑞克林对局灶性脑缺血再灌注损伤大鼠有神经保护作用,其机制可能与抑制p38MAPK活化、减少神经细胞凋亡有关。
Objective To investigate the neuroprotective effect of urokallikrein on a cerebral ischemia-reperfusion injury model of rat.Methods Sixty male adult Sprague-Dawley rats were randomly assigned into three groups： a sham operation group（sham group）,focal cerebral ischemia-reperfusion group（model group）,and urokallikrein group.The middle cerebral artery occlusion reperfusion model was made by the suture method（ischemia for 2 hours,and reperfusion for 24 hours）.After that,the rats were sacrificed by decapitation,the neurological function was evaluated,the pathological change was observed after HE staining,the expression of p38MAPK phosphorylation was detected by the immunohistochemical method,and apoptotic cells were measured by the TUNEL method 24 hours after ischemia-reperfusion injury.Results Compared with the sham group,the neurological function score was increased,the cell injury（HE staining） was more severe,the number of positive p-p38 cells and positive TUNEL cells were increased in rats after ischemia-reperfusion injury,the difference between the two groups was significant（P0.01）.Compared with the model group,urokallikrein reduced the neurological function score,attenuated cell injury,and reduced the number of positive p-p38 cells and positive TUNEL cells.The difference between the two groups was significant（P0.01）.Conclusions Urokallikrein has a neuroprotective effect on cerebral ischemia-reperfusion injury in rats,and its mechanism may be related to attenuating p38MAPK pathway and inhibiting neuronal apoptosis.
出处
《中国校医》
2013年第6期439-442,F0003,共5页
Chinese Journal of School Doctor
