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目的：探讨红景天苷(Sal)对高原缺氧大鼠认知功能障碍的治疗作用及其可能机制。方法：将30 只成年雄性SD 大鼠随机分为健康对照组、模型组(Model 组) 、Sal[按体重1g/ (kg·d) ]治疗组(sal 组)。采用Morris 水迷宫实验方法检测缺氧后大鼠学习记忆功能变化，同时检测脑组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽(GSH)、丙二醛(MDA)的水平。结果：(1) 模型组大鼠寻找平台的潜伏期明显长于对照组，具有统计学意义( P < 0.05)，Sal 组寻找平台的潜伏期相对于模型组显著缩短( P < 0.05)。撤离平台后，模型组大鼠在平台所在象限的停留时间明显短于对照组( P < 0.05)，Sal 治疗后大鼠在平台所在象限的停留时间较模型组显著延长( P < 0.05)。(2) 模型组SOD、GSH-PX、GSH 显著下降，MDA 明显增高，Sal 干预组SOD、GSH-PX、 GSH 显著增高,而MDA 明显下降，具有统计学意义(P<0.05)。结论：Sal 可改善高原缺氧大鼠认知功能，其可能机制是通过减轻海马区的氧化应激反应减轻海马区的损伤，从而实现改善认知功能。

英文摘要:

Objective: To investigate the effects of salidroside (Sal) on cognitive deficits induced by hypobaric hypoxia and to investigate the possible mechanism in terms of oxidative stress in hippocampus. Methods: A total of 30 male Sprague-Dawley rats (200± 20g) were randomly divided into three groups: (n =10 in each group): Control group, Model group and Sal group. Severe cognitive deficits were tested by the water maze task. The content of Glutathione(GSH) and Maleic Dialdehyde(MDA) were measured; The activity of Superoxide Dismutase (SOD) and glutathione peroxidase (GSH-PX)in the homogenate of Hippocampus were detected. Results: Hypobaric hypoxia can cause severe cognitive deficits, and salidroside could attenuate hypobaric hypoxia-induced cognitive deficits. Biochemical experiments revealed that hypobaric hypoxia can significantly increase MDA, decrease GSH and the activities of SOD and GSH-PX in the homogenate of Hippocampus, which can be reversed by salidroside. Conclusions: Salidroside exhibits therapeutic potential for hypobaric hypoxia-induced cognitive deficits, which may be related to its anti-oxidative stress actions in hippocampus.

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