[關(guān)鍵詞]
[摘要]
目的 研究3,5-二咖啡?？鼘幩釋?duì)大鼠實(shí)驗(yàn)性局灶性腦缺血-再灌注損傷模型的保護(hù)作用。方法 采用線栓法阻塞大鼠腦中動(dòng)脈（MCAO）制備局灶性腦缺血-再灌注損傷模型，觀察3,5-二咖啡?？鼘幩釋?duì)模型大鼠狀態(tài)、神經(jīng)行為學(xué)的影響，以及對(duì)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(guò)氧化物酶（GSH-Px）、過(guò)氧化氫酶（CAT）、一氧化氮（NO）和一氧化氮合酶（NOs）的影響。結(jié)果 3,5-二咖啡?？鼘幩釀?.13、18.25 mg/kg時(shí)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(qiáng)T-SOD、CAT、GSH-Px的活性（P＜0.05）。結(jié)論 3,5-二咖啡?？鼘幩釋?duì)腦缺血-再灌注損傷有較好的保護(hù)作用，其作用機(jī)制可能與抗自由基生成有關(guān)。
[Key word]
[Abstract]
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.
[中圖分類(lèi)號(hào)]
[基金項(xiàng)目]
國(guó)家自然科學(xué)基金資助項(xiàng)目（30672602；81102895）；四川省中醫(yī)藥管理局學(xué)術(shù)和技術(shù)帶頭人專(zhuān)項(xiàng)（2007XS21）；四川省教育廳自然科學(xué)重點(diǎn)項(xiàng)目（07ZA024）
