目的 研究3,5-二咖啡?？鼘幩釋Υ笫髮嶒炐跃衷钚阅X缺血-再灌注損傷模型的保護作用。方法 采用線栓法阻塞大鼠腦中動脈（MCAO）制備局灶性腦缺血-再灌注損傷模型，觀察3,5-二咖啡酰奎寧酸對模型大鼠狀態(tài)、神經行為學的影響，以及對腦梗死比率及血清中丙二醛（MDA）、總超氧化物歧化酶（T-SOD）、谷胱甘肽過氧化物酶（GSH-Px）、過氧化氫酶（CAT）、一氧化氮（NO）和一氧化氮合酶（NOs）的影響。結果 3,5-二咖啡酰奎寧酸劑9.13、18.25 mg/kg時均能明顯降低模型大鼠腦梗死的比率（P＜0.05），降低血清中MDA水平（P＜0.01），增強T-SOD、CAT、GSH-Px的活性（P＜0.05）。結論 3,5-二咖啡?？鼘幩釋δX缺血-再灌注損傷有較好的保護作用，其作用機制可能與抗自由基生成有關。

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.

國家自然科學基金資助項目（30672602；81102895）；四川省中醫(yī)藥管理局學術和技術帶頭人專項（2007XS21）；四川省教育廳自然科學重點項目（07ZA024）