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作 者:史高峰[1] 杨军英[2] 鲁润华[1] 李春雷[3] 杨云裳[1] 杨爱梅[1]
机构地区:[1]中国科学院兰州化学物理研究所,甘肃兰州730000 [2]兰州医学院药理学教研室,甘肃兰州730000 [3]兰州理工大学化工学院,甘肃兰州730050
出 处:《中国药理学通报》2005年第2期206-209,共4页Chinese Pharmacological Bulletin
摘 要:目的 研究 1, 5, 8 trihydroxy 3 methoxy xanthoneXanth对大鼠局灶性脑缺血再灌注损伤的保护作用。方法 采用线栓法阻断大脑中动脉 (MCA)血流,造成局灶性脑缺血再灌注模型;评价大鼠行为功能、测定脑梗死体积及脑血清中丙二醛(MDA)含量、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)活性。结果 1, 5, 8 trihydroxy 3 methoxy xanthone对大鼠脑缺血再灌注的模型组与假手术组相比,MDA含量升高 (P<0 05 ),SOD、GSH Px的活力降低 (P<0 05)。Xanth两剂量组与模型组相比MDA含量降低 (P<0 05),SOD、GSH Px的活力升高 (P<0 05)。结论 1, 5, 8 trihydroxy 3 methoxy xanthone对大鼠脑缺血再灌注损伤具有保护作用,其作用机制可能与保护SOD、GSH Px的活性,减少脂质过氧化有关。Aim To study the protective effects of 1,5,8-trihydro xy-3-methoxy-xanthone (Xanth) on focal cerebral ischemia reperfusion injury in rats. Methods Focal cerebral ischemia was made by middle cerebral artery occlusion for 4 h a nd reperfusion for 1h. Neurological deficit and infarcts were observed, and the content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) a nd GSH-Px were measured after ischemia-reperfusion.Results Th e content of MDA in ischemic rats was increased (P<0.05), while the activit ies of SOD, GSH-Px significantly decreased. Xanth.at 10 and 20 mg·kg -1 d ecreased the content of MDA, while increased the activities of SOD, GSH-Px (P <0.05).Conclusion 1,5,8-trihydroxy-3-methoxy-xanthone has protective effect against cerebral ischemia reperfusion injury by protecting SOD and GSH-Px activities and reducing the lipid per-oxidation.
关 键 词:1 5 8-trihydroxy-3-methoxy-xanflmne 脑缺血再灌注损伤 丙二醛 超氧化物歧化酶 谷胱甘肽过氧化物酶
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