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机构地区:[1]兰州大学第二医院超声科,兰州730030 [2]兰州大学第二医院药剂科,兰州730030 [3]兰州大学药学院,兰州730000
出 处:《中国新药杂志》2008年第16期1399-1401,1428,共4页Chinese Journal of New Drugs
基 金:甘肃省自然科学基金资助项目(32s061-A25-101)
摘 要:目的:研究红毛五加总苷(total glucosides ofAcanthopanax giraldiiHarms,TGA)对实验性脑缺血的保护作用,初步探讨其作用机制。方法:采用结扎双侧颈总动脉致大、小鼠脑缺血模型,检测脑缺血小鼠的存活时间及脑缺血大鼠的脑毛细血管通透性、脑指数、脑含水量及脑组织乳酸(LA)、丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果:TGA能明显延长脑缺血小鼠的存活时间,能显著降低脑缺血大鼠的脑毛细血管通透性、脑指数、脑含水量及脑组织LA、MDA含量,并提高SOD活性。结论:TGA对结扎双侧颈总动脉致大、小鼠脑缺血具有明显保护作用,作用机制可能与其降低LA性酸中毒与增强抗氧化作用有关。Objective: To study the protective effects of total glucosides of Acanthopanax giraidii Harms (TGA) on experimental cerebral ischemia and its mechanism. Methods: Cerebral ischemia was induced by bilateral common carotid artery occlusion in mice and rats. The survival time of cerebral ischemic mice was recorded, the cerebral capillary permeability, cerebral index, cerebral water content, the content of lactic acid (LA) and malondialdehyde ( MDA), and the activity of superoxide dismutase (SOD) in the brain were determined in cerebral ischemic rats. Results: TGA prolonged the survival time of cerebral ischemic mice. It also reduced the cerebral capillary permeability, cerebral index and cerebral water content of cerebral ischemic rats. TGA decreased LA and MDA contents and increased SOD activity of the brain in cerebral ischemic rats. Conclusion: TGA possesses the protective effects on cerebral ischemia in mice and rats; its mechanisms may relate to decrease of LA content and increase of antioxidation.
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