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作 者:孙峰[1] 刘颖菊[1] 肖小华[1] 高丽佳[1]
机构地区:[1]重庆医科大学药理教研室重庆市生物化学与分子药理重点实验室,重庆400016
出 处:《中国老年学杂志》2006年第10期1363-1365,共3页Chinese Journal of Gerontology
基 金:重庆市科技攻关项目(CSTC2005AC0120)
摘 要:目的研究羟基积雪草甙(madecassoside,MC)对慢性铝中毒痴呆小鼠的保护作用。方法葡萄糖酸铝按铝400 mg.kg-1.d-1灌胃90 d建立慢性铝中毒痴呆小鼠模型。通过HE染色、Morris水迷宫试验和生化实验,观察MC三种剂量(30、60和120 mg.kg-1.d-1)同步给药90d对小鼠海马神经元损伤、空间学习记忆能力和脑组织单胺氧化酶B(MAO-B)活性的影响。结果与模型组比较,30和60 mg.kg-1.d-1MC明显减轻铝过负荷所致的海马神经元损伤,明显缩短小鼠寻找平台潜伏期(s)(35.9±10.9 vs 16.5±8.4和19.6±10.5)(P<0.05);同时三种剂量MC均明显降低小鼠脑组织中MAO-B活性(U.h-1.mg-1prot)(18.9±1.8 vs 14.6±1.7,13.7±2.3和13.6±1.4)(P<0.05)。结论MC对慢性铝中毒小鼠海马神经元有保护作用,改善痴呆小鼠学习记忆能力。Objective To study the ameliorative effects of madecassoside(MC) on dementia induced by long-term intake of aluminum in mice. Methods The dementia mice models were made by given with AI 400 mg mg·kg^-1·d^-1 for 90 days. The ameliorative effects of MC(30, 60 and 120 mg·kg^-1·d^-1) on hippocampases neuron degeneration, spatial learning and memory retention and the activity of monoamine oxidase-B (MAO-B) were detected by HE staining and Momis water maze tests and biochemistry. Results Compared with model group, MC 30 and 60 mg·kg^-1·d^-1 improved pathological morphology of hippocampus neurons and reduced escape latency of mice trained in the Morris water maze task significantly (s) (35.9 ± 10.9 vs 16.5 ±8.4 and 19.6 ±10.5) ( P 〈 0.05) ; All dosages of MC inhibited the activities of MAO-B in brain significantly ( U ·h^-1 mg^-1 prot) ( 18.9 ± 1.8 vs 14.6 ±1. 7,13.7 ± 2.3 and 13.6 ± 1.4) ( P 〈 0.05 ). Conclusions MC could protect the neurons of hippocampus from the chronic aluminum toxicities and ameliorate the ability of spatial learning and memory in dementia mice.
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