中文摘要：

目的研究3,5-二咖啡酰奎宁酸对大鼠实验性局灶性脑缺血-再灌注损伤模型的保护作用。方法采用线栓法阻塞大鼠脑中动脉（MCAO）制备局灶性脑缺血．再灌注损伤模型，观察3，5-二咖啡酰奎宁酸对模型大鼠状态、神经行为学的影响，以及对脑梗死比率及血清中丙二醛（MDA）、总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH．Px）、过氧化氢酶（CAT）、一氧化氮（NO）和一氧化氮合酶（NOs）的影响。结果3，5-二咖啡酰奎宁酸剂9．13、18．25mg／kg时均能明显降低模型大鼠脑梗死的比率（P〈0．05），降低血清中MDA水平（P〈0．01），增强T-SOD、CAT、GSH．Px的活性（P〈0．05）。结论3，5-二咖啡酰奎宁酸对脑缺血．再灌注损伤有较好的保护作用，其作用机制可能与抗自由基生成有关。

英文摘要：

Objective To research the protection of 3,5-dicaffeoylquinic acid on cerebral ischemia-reperfusion injury in rats. Methods： Rat model of focal cerebral ischemia-reperfusion injury was created by the middle cerebral artery occlusion （MCAO） by modified suture method. The effect of 3,5-dicaffeoylquinic acid on model rats was investigated for. the neuroethology, the rate of cerebral infarction area, the content or activity of malondialdehyde （MDA）, total superoxide dismutase （T-SOD）, glutathione peroxidase （GSH-px）, catalase （CAT）, nitrogen oxide （NO） ,and nitricoxide synthase （NOs） in serum, using Nimodipine as the positive control drug. Results： 3,5-Dicaffeoylquinic acid with the doses of 9.13 and 18.25 mg/kg could obviously increase the rate of the cerebral infarction area in MCAO rats （P〈0.05） as well as MDA level （P〈0.01） while increase the activity ofT-SOD, CAT, and GSH-Px in serum （P〈0.05）. Conclusion： 3,5-Dicaffeoylquinic acid, exerts a better effect on cerebral ischemia-reperfusion injury in rats and its mechanism may be related to the generation of anti-free radical.