摘要
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。
Objective： To investigate the effects ofsalidroside （Sal） on cognitive deficits induced by hypobaric hypoxia and to in- vestigate 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： Hypo- baric 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.
出处
《现代生物医学进展》
CAS
2011年第11期2026-2029,共4页
Progress in Modern Biomedicine
