目的 研究珍龙醒脑胶囊对大鼠局灶性脑缺血再灌注损伤的保护作用。方法 120只SD大鼠随机分为假手术组, 模型组, 尼莫地平(37 mg/kg)组, 珍龙醒脑胶囊低、高剂量(125、250 mg/kg)组。利用大鼠可逆性右侧脑中动脉闭塞线栓法制作局灶性脑缺血再灌注模型, 用Longa's法、TTC染色法评价大鼠的神经功能评分和脑梗死体积;检测左右半脑组织中谷胱甘肽(GSH)、总抗氧化能力(T-AOC)、总超氧化物歧化酶(T-SOD)、丙二醛(MDA)的量;Western blotting法检测脑组织中P38、NF-κB、Bcl-2、Bax、Caspase-3蛋白表达水平。结果 与假手术组比较, 模型组大鼠神经功能症状评分、脑梗死体积显著增高, T-AOC、T-SOD水平降低, 同时促进P38和Caspase-3蛋白表达。与模型组比较, 珍龙醒脑胶囊低、高剂量组及尼莫地平组可显著降低脑缺血再灌注大鼠的神经功能评分, 减少脑梗死体积, 提高T-AOC、T-SOD水平, 珍龙醒脑胶囊高剂量组可抑制P38和Caspase-3的蛋白表达。结论 珍龙醒脑胶囊对大鼠脑缺血再灌注损伤具有明显的保护作用, 其机制可能与改善神经功能、减少自由基损伤和抑制炎症因子表达和细胞凋亡有关。

Objective To study the protective effect of Zhenlong Xingnao Capsule (ZXC) on the cerebral ischemia-reperfusion injury of rats. Methods Total 120 Sprague-Dawley (SD) rats were randomly divided into Sham operation group, the middle cerebral artery occlusion (MCAO) model group, Nimodipine (37 mg/kg BW) group, low-dose ZXC (125 mg/kg) group, and high-dose ZXC (250 mg/kg). A focal cerebral ischemia-reperfusion model was made by using the occlusion of MCAO and occlusion of the right middle cerebral artery in rats. The infarct volume and the neurological deficit were determined by TTC staining and Longa's score; And to determine the contents of GSH, T-AOC, T-SOD, and MDA in left and right half brain tissues. To detect the protein expression level changes of P38, NF-κB, Bcl-2, Bax, and Caspase-3 by Western blotting method. Results Compared with the Sham operation group, the neurologic symptom scores and infarct volume of MCAO of rats in model group were significantly increased, and the vigor of T-AOC and T-SOD was decreased. At the same time the protein expression of P38 and Caspase-3 was promoted. Compared with the model group, the neurologic symptom scores, injury degree of brain tissues, and brain infarct volume of rats with cerebral ischemia-reperfusion injury were significantly decreased in the Nimodipine, low-dose ZXC, and high-dose ZXC groups, the vigor of T-SOD and T-AOC was increased. The high-dose ZXC can inhibit P38 and Caspase-3 expressions. Conclusion ZXC has the obvious protective effect on the brain ischemia-reperfusion injury in rats. Its mechanism may be related to the improvement of neurological function, the reduction of free radical injury, the inhibition of inflammation and the cell apoptosis.