【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。更多还原

【Abstract】 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 Al 400 mg·kg^-1·d^-1 for 90 days.The ameliorative effects of MC(30,60 and 120 mg·kg^-1·d^-1)on hippocampuses neuron degeneration,spatial learning and memory retention and the activity of monoamine oxidase-B（MAO-B） were detected by HE staining and Morris 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.更多还原