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、18.25 mg/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。

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 of T-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.

国家自然科学基金资助项目（30672602；81102895）；四川省中医药管理局学术和技术带头人专项（2007XS21）；四川省教育厅自然科学重点项目（07ZA024）