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红景天苷对癫痫大鼠认知功能障碍的治疗作用及其可能机制
引用本文:杨江河,魏敏,张蓉,李华,闫志强,刘绍明.红景天苷对癫痫大鼠认知功能障碍的治疗作用及其可能机制[J].生物磁学,2011(15):2868-2871.
作者姓名:杨江河  魏敏  张蓉  李华  闫志强  刘绍明
作者单位:[1]兰州军区乌鲁木齐总医院神经外科,新疆乌鲁木齐830000 [2]克孜勒苏军分区卫生所,新疆阿图什市844200 [3]兰州军区乌鲁木齐总医院妇产科,新疆乌鲁木齐830000
摘    要: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。

关 键 词:癫痫持续状态  红景天苷  认知功能障碍

Salidroside for Epilepticus-Induced Cognitive Deficits in Rats and Its Possible Mechanism
YANG Jiang-hes,WEI Min,ZHANG Rong,LI Hua,XIU Bin-hua,YAN Zhi-qiangs,LIU Shao-ming.Salidroside for Epilepticus-Induced Cognitive Deficits in Rats and Its Possible Mechanism[J].Biomagnetism,2011(15):2868-2871.
Authors:YANG Jiang-hes  WEI Min  ZHANG Rong  LI Hua  XIU Bin-hua  YAN Zhi-qiangs  LIU Shao-ming
Affiliation:1 department of neurosurgery , Utumchi Hospital of Lanzhou Military region, Ummchi 830000, China ; 2 Infirmary of Kezilesu Military Subregion in Xinjiang, Atushi 844200, China; 3 department ogynaecology and obstetrics, Urumchi Hospital oLanzhou Military region, Urumchi 830000, China)
Abstract:Objective: The purpose of the study was to investigate the effects of Salidroside (Sal) on cognitive deficits induced by status epilepticus (SE) and the possible mechanism in terms of oxidative stress in hippocampus. Methods: A total of 24 male Sprague-Dawley rats (220± 30 g) were randomly assigned to one of the following groups: (n =8 in each group): Control group,Model group and Sal group. Severe cognitive deficits in lithium-pilocarpine seizure model was tested by the water maze task. Glutathione(GSH) and Maleic Dialdehyde(MDA) content of the homogenate of Hippocampus were measured; The activity of Superoxide Dismutase (SOD) and glutathione peroxidase (GSH-PX)in the homogenate of Hippocampus were detected. Results: SE can cause severe cognitive deficits, and Sal could attenuate SE-induced cognitive deficits. Biochemical experiments revealed that SE can significantly increase content of MDA, decrease content of GSH and decreased the activities of SOD and GSH-PX in the homogenate of Hippocampus, which can be reversed by Sal. Conclusions: Sal exhibits therapeutic potential for SE-induced cognitive deficits, which is most likely related to its anti-oxidative stress actions in hippocampus.
Keywords:Status epilepticus  Salidroside  Cognitive deficits
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