[1]肖小华,张静,杨俊卿.慢性铝过负荷致大鼠认知功能损伤及尼莫地平保护作用观察[J].第三军医大学学报,2007,29(11):1028-1031.
 XIAO Xiao-hua,ZHANG Jing,YANG Jun-qing.Neurotoxicity of chronic aluminum overload and protective effects of nimodipine in rats[J].J Third Mil Med Univ,2007,29(11):1028-1031.
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慢性铝过负荷致大鼠认知功能损伤及尼莫地平保护作用观察
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第11期
页码:
1028-1031
栏目:
论著
出版日期:
2007-06-15

文章信息/Info

Title:
Neurotoxicity of chronic aluminum overload and protective effects of nimodipine in rats
作者:
肖小华 张静 杨俊卿
重庆医科大学:护理系药理学教研室,药学院药理学教研室
Author(s):
XIAO Xiao-hua ZHANG Jing YANG Jun-qing
Department of Pharmacology of Nursing Faculty,Department of Pharmacology of College of Pharmacy, Chongqing Medical University, Chongqing 400016, China
关键词:
慢性铝过负荷认知功能损伤MAO-B氧化应激尼莫地平
Keywords:
chronic aluminum overload cerebral damage MAO-B oxide stress nimodipine
分类号:
R155.33; R338.64; R972
文献标志码:
A
摘要:
目的    观察铝过负荷对大鼠的神经毒性及尼莫地平的保护作用。    方法    大鼠灌胃给予葡萄糖酸铝(Al3+ 400 mg/kg),1次/d,1周5 d,持续12周,建立慢性铝负荷致大鼠脑损伤、神经元退变模型。观察指标包括行为学(跳台法测定被动回避性学习记忆能力、水迷宫测定空间定向能力)、组织病理学、生化酶学(MAO-B、ChAT、AchE和SOD活性,MDA含量)等,尼莫地平(80 mg/kg)或者生理盐水在给予铝盐后4 h灌胃给予。    结果     与对照组相比,慢性铝过负荷明显导致大鼠被动回避性学习记忆能力和空间定向能力障碍、大鼠海马神经元明显核固缩和数目减少;海马ChAT、SOD活性明显降低,AchE、MAO-B活性、MDA含量明显升高;尼莫地平给予能明显改善铝负荷大鼠的学习记忆能力损害和海马神经元损伤。    结论    铝过负荷致大鼠脑损伤、学习记忆能力障碍可能涉及细胞内钙超载、氧化应激损伤以及MAO-B活性改变;尼莫地平对慢性铝负荷的神经毒性有明显的保护作用。
Abstract:
Objective    To study the neurotoxicity of chronic aluminum overload and the protective effects of nimodipine in rats.     Methods    The brain damage models of rats were established via intragastric administration of aluminum gluconate(element aluminum 400 mg/kg) once a day, 5 d/week for 12 weeks. The step-down test and programmed Morris water maze test were used to evaluate the changes of learning and memory functions of rats.  Pathomorphological changes of hippocampi of rats were observed.  The activities of SOD, ChAT, AchE, MAO-B and the contents of MDA of brain tissue in rats were also measured.  Nimodipine (80 mg/kg) were intragastrically administered 4 h after aluminum administration every time for 12 weeks.      Results    Chronic aluminum administration induced the impairment of avoidance learning and memory ability and spatial oriental ability.  Consistent with the behavioral changes, neuronal death in the hippocampi, decreased activities of SOD and ChAT, increased content of MDA, and increased activity of MAO-B and AchE were detected in the aluminum-overload mice.  The administration of nimodipine could significantly protect rats from the brain damage, and behavioral and biochemical changes above caused by aluminum overload were in a dose-dependent manner.     Conclusion    These results suggest that changes of cellular calcium overload and oxide stress and   MAO-B activities are involved in pathophysiological mechanisms of brain injury induced by chronic aluminum overload.  Nimodipine has a protective effect on neurotoxicity of chronic aluminum overload.

参考文献/References:

肖小华, 张静, 杨俊卿. 慢性铝过负荷致大鼠认知功能损伤及尼莫地平保护作用观察[J]. 第三军医大学学报, 2007, 29(11):1028-1031.

更新日期/Last Update: 2008-10-23