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机构地区:[1]河北北方学院药学系
出 处:《神经药理学报》2011年第6期1-6,共6页Acta Neuropharmacologica
基 金:国家自然科学基金项目(No.81073120);河北省自然科学基金项目(No.C2009001026);河北省科技攻关计划项目(No.07276166);河北省教育厅项目(No.2010212)
摘 要:目的:研究大黄素对脑缺血再灌注小鼠记忆功能的保护作用。方法:采用改进的Himori法暂时性阻断小鼠两侧颈总动脉制备脑缺血再灌注损伤模型,进行避暗实验、穿梭实验、常压耐缺氧实验、断头耐缺氧实验和亚硝酸钠中毒耐缺氧实验,观察大黄素(10.0,1.0,0.1 mg·kg-1,ip)对脑缺血再灌注小鼠记忆功能和耐缺氧能力的影响,并对各剂量组小鼠脑组织和血液中谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-PX)活力和超氧化物歧化酶(superoxide dismutase,SOD)活力进行测定。结果:大黄素可改善脑缺血再灌注损伤所致的记忆功能障碍,明显延长小鼠耐缺氧生存时间,增加GSH-PX和SOD活力。结论:大黄素对脑缺血再灌注损伤小鼠记忆功能有保护作用,其作用机制可能是通过增强抗氧化酶GSH-PX和SOD活力,提高脑组织对氧自由基的清除能力和耐缺氧能力,从而减轻缺血再灌注引起的脑组织损伤。Objective: To study the protective effects of emodin on the memory of mice experiencing cerebral ischemia reperfusion and their underlying mechanisms. Methods: Using improved Himori method, cerebral ischemia reperfusion injury was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. The protective effects of emodin (10.0, 1.0, 0.1 mg·kg-1,ip) on the memory of the model mice were examined using the step-through test, shuttle box test, antihypoxia test under normal pressure, test of acute cerebral hypoxia induced by decapitated mice and test of NaNO2 histotoxic anoxia. Meanwhile, the superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-PX) activity were also measured. Results: Emodin could attenuate the memory impairment induced by cerebral ischemia reperfusion injury, prolong the antihypoxic survival time, and increase the activities of GSH-PX and SOD. Conclusions:Emodin showed protective effects on the memory of mice with cerebral ischemia reperfusion injury. The possible mechanism may involve the enhancement of the activities of GSH-PX and SOD, which leads to the increased oxygen free radicals scavenging ability, enforced antihypoxic capacity and alleviation of cerebral ischemia damage.
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