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王月古,汪弢,邱昕,梅瑰,冯佩,陈国华.黄连解毒汤对APP/PS1双转基因阿尔茨海默病小鼠自由基代谢及海马区病理形态学影响[J].,2011,31(10):1379-1382
黄连解毒汤对APP/PS1双转基因阿尔茨海默病小鼠自由基代谢及海马区病理形态学影响
Effects of Huanglian Jiedu Decoction on Free Radicals Metabolism and Pathomorphism of the Hippocampus in APP/PS1 Double Transgenic Mice
  
DOI:
中文关键词:  黄连解毒汤  阿尔茨海默病  APP/PS1双转基因小鼠  老年斑  自由基
英文关键词:Huanglian Jiedu Decoction  Alzheimer’s disease  APP/PS1 double transgenic mice  senile plaque  free radical
基金项目:湖北省自然科学基金资助项目(No.2007ABA060)
Author NameAffiliation
王月古 华中科技大学同济医学院附属中西医结合医院神经内科 
WANG Tao 华中科技大学同济医学院附属中西医结合医院神经内科 
QIU Xin 华中科技大学同济医学院附属中西医结合医院神经内科 
梅瑰 华中科技大学同济医学院附属中西医结合医院神经内科 
冯佩 华中科技大学同济医学院附属中西医结合医院神经内科 
CHEN Guo-hua 华中科技大学同济医学院附属中西医结合医院神经内科 
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中文摘要:
      目的观察黄连解毒汤对阿尔茨海默病(Alzheimer’s disease,AD)模型小鼠自由基代谢及海马CA1区的神经细胞形态学、组织病理学的影响,并探讨其可能治疗机制,为黄连解毒汤治疗AD提供实验依据。方法采用APP/PS1双转基因AD小鼠模型,随机分为模型对照组、阳性对照组(安理申)、黄连解毒汤大剂量组[865mg/(kg.d)]、黄连解毒汤中剂量组[433mg/(kg.d)]、黄连解毒汤小剂量组[216mg/(kg.d)],每日予以相应药物灌胃治疗7个月后,于10月龄检测自由基代谢指标超氧化物歧化酶(SOD)及丙二醛(MDA),观察各组干预措施对小鼠海马区CA1区神经细胞形态学及老年斑的影响。结果各用药组均能明显提高SOD,降低MDA含量(P<0.05),减少神经细胞的破坏、老年斑的形成,有效阻止海马神经细胞的退变,黄连解毒汤中剂量组优于安理申组(P<0.05)。结论黄连解毒汤治疗AD的机制可能与提高抗氧化能力,保护海马神经细胞,减少老年斑的生成等机制相关。
英文摘要:
      Objective To observe the effects of Huanglian Jiedu Decoction(HLJDT) on the metabolism of free radicals,the morphology and histopathology of hippocampal CA1 neurons in PS1/APP double transgenic mice of Alzheimer’s disease(AD),and to study its possible mechanisms,thus providing experimental evidence for treating AD by HLJDT.Methods The APP/PS1 double transgenic mouse model was used.Mice were randomly divided into five groups,i.e.,the model control group,the positive control group(Aricept),high-,middle-,and low-dose HLJDT group(at the daily dose of 865 mg·kg-1,433 mg·kg-1,and 216 mg·kg-1,respectively).Corresponding medication was daily given by gastrogavage.Seven months later superoxide dismutase(SOD) and malondialdehyde(MDA) were detected at the ten-month old mice,thus observing the effects on the morphology of CA1 hippocampal neurons and the senile plaques(SP).Results HLJDT and Aricept could obviously increase the SOD contents and lower the MDA contents(P<0.05),attenuate the destroy of neurocytes and the formation of SP,effectively hinder the degeneration of hippocampal neurons.Better results were obtained in the middle-dose HLJDT group than in the positive control group(P<0.05).Conclusion The mechanism of HLJDT in treating AD might be possibly correlated with improving anti-oxygenation,protecting hippocampal neurocytes,and reducing the formation of SP.
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