中文摘要：

目的探讨丹龙醒脑方对局灶性脑缺血再灌注大鼠大脑皮质半暗带（ischemic penumbya,IP）区神经细胞凋亡与即早基因c-fos、c-jun、c-myc表达的关系。方法将48只雄性SD大鼠随机均分为假手术组,脑缺血再灌注（模型）组,尼莫地平组及丹龙醒脑方小、中、大剂量组（丹小组、丹中组、丹大组）。后五组用线栓法制备大脑中动脉栓塞再灌注（MCAO/R）模型,再灌注24 h进行神经功能缺损评分后,取缺血侧大脑皮质,采用原位末端标记法（TUNEL）检测凋亡的神经细胞,免疫组化法分别检测c-fos、c-jun、c-myc蛋白。结果与假手术组比较,其余各组的神经功能缺损评分、神经细胞凋亡指数（AI）及cfos、c-jun、c-myc蛋白的积分光密度（IOD）值均升高,差异有统计学意义（P〈0.05,P〈0.01）;与模型组比较,尼莫地平组和丹龙醒脑方各剂量组的神经功能缺损评分、神经细胞AI及c-fos、c-jun、c-myc蛋白的IOD值均减小,差异有统计学意义（P〈0.05,P〈0.01）;尼莫地平组、丹龙醒脑方各剂量组组间比较,各指标差异均无统计学意义（P〉0.05）。结论丹龙醒脑方能显著降低脑缺血后神经功能缺损和减少神经细胞凋亡,其机制可能与下调即早基因c-fos、c-jun和c-myc的表达有关。

英文摘要：

Objective To investigate the relationship of Danlong Xingnao Prescription（DLXNP） on neural cell apoptosis and expression of c-fos, c-jun and c-myc in ischemic penumbra of rats with cerebral ischemia-reperfusion injury（MCAO/R）.Methods 48 male SD rats were randomly divided into the sham-operation group, cerebral ischemia-reperfusion injury（model） group, nimodipine group, small, medium, high dose of DLXNP groups. The middle cerebral artery occlusion/ reperfusion models were prepared by suture method. The neural function defect scale was evaluated after 24 hours of reperfusion, researchers carried out, and the ischemic side of brain cortex was taken out. The nerve cells of apoptosis were detected by using terminal-deoxynucleoitidyl transferase mediated nick end labeling（TUNEL） method, and the expression of c-fos, c-jun and c-myc was determined by immunohistochemistry. Results Compared with the operation group, the neural function defect scale,apoptotic index（AI） and integrated optical density（IOD） of c-fos, c-jun, c-myc were increased, the differences were statistically significant（P〈0.05, P〈0.01）. Compared with model group, the neural function defect scale, AI and IOD of c-fos, c-jun, c-myc in nimodipine group and DLXNP groups were reduced（P〈0.05, P〈0.01）; The defferences between nimodipine group and different doses of DLXNP groups were not statistically significant in all indicators（P〈0.05）. Conclusion Danlong Xingnao pecipe can lower the neural function defect and reduced neural cell apoptosis, which may relate to the down-regulated expression of c-fos, c-jun and c-myc.