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目的:探讨红景天苷(Sal)对癫痫大鼠认知功能障碍的治疗作用及其可能机制。方法:将24只成年雄性SD大鼠随机分为健康对照组、模型组、Sal[按体重1g/(kg·d)]干预组。采用Morris水迷宫方法检测大鼠学习记忆功能变化,并检测大鼠脑组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和谷胱甘肽(GSH)、丙二醛(MDA)相应的比酶活力及含量变化。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、GSH-PX显著下降,MDA明显增高,Sal干预组SOD、GSH、GSH-PX明显增高,而MDA显著下降,有统计学差异(P<0.05)结论:Sal可减轻癫痫持续状态所致的认知功能障碍,其可能机制是通过减轻海马区氧化应激减轻海马区的损伤,进而改善认知功能。
Objective: To investigate the therapeutic effect of salidroside (Sal) on cognitive dysfunction in epileptic rats and its possible mechanism. Methods: Twenty-four adult male Sprague-Dawley rats were randomly divided into a healthy control group, a model group, and a Sal [1 g/(kg·d)] intervention group. The Morris water maze test was used to detect the changes of learning and memory function in rats, and the superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and glutathione (GSH) in the rat brain were detected. The corresponding specific enzyme activity and content of malondialdehyde (MDA) were changed. Results: (1) The latent period of the platform for rats in the model group was significantly longer than that of the control group (P<0.05), and the latent period for finding the platform in the Sal group was significantly shorter than that in the model group (P<0.05). After evacuation from the platform, the residence time of the model group rats in the quadrant of the platform was significantly shorter than that of the control group (P<0.05). After the Sal treatment, the residence time of the rats in the quadrant of the platform was significantly longer than that of the model group (P<0.05). (2) SOD, GSH and GSH-PX in the model group decreased significantly and MDA significantly increased. The SOD, GSH and GSH-PX in the Sal intervention group increased significantly, while the MDA decreased significantly (P<0.05). Conclusion: Sal can To reduce the cognitive dysfunction caused by status epilepticus, the possible mechanism is to reduce the damage of the hippocampus by reducing the oxidative stress in the hippocampus, and then improve the cognitive function.