灵芝三萜类化合物对AD大鼠脑海马神经细胞Aβ_(1-40)的影响  

Effects of the expression of Aβ1-40in Alzheimer disease of the model animals through Ganoderma Lucidum Triterpenoids

作　　者：张玥[1] 罗俊[1] 黄能慧[1] 张小毅[1] 

机构地区：[1]贵州医科大学药理学教研室,贵州贵阳550004

出　　处：《贵州医药》2016年第7期681-682,共2页Guizhou Medical Journal

基　　金：教育部科学技术研究重点项目(V200801);贵州省科技攻关项目(黔科合2004NGY031);贵州省优秀科技教育人才省长专项资金(2005293)

摘　　要：目的研究灵芝三萜类化合物(GLT)对阿尔茨海默病(AD)大鼠脑海马神经细胞Aβ1-40表达的影响。方法将自然衰老模型大鼠60只随机均分为六组:模型组,GLT低、中、高剂量组,溶媒对照组(食用油)及阳性对照组(健脑胶囊),5个月龄大鼠10只为正常对照组。连续灌胃给药60d后,免疫组化法检测海马Aβ1-40表达。结果模型组海马神经细胞Aβ_(1-40)表达增多,GLT组Aβ_(1-40)表达减少。结论 GLT有防治AD的作用,其作用机制可能与减轻Aβ的神经毒性以及减少脑内Aβ沉积有关。Objective To observe the effects of the expression of Aβ1-40 in Alzheimer Disease （AD） of model ani- mals by used the Ganoderma Lucidum Triterpenoids （GLT）. Methods 60 natural aging rats were randomly divided into 6 groups which were GLT low dose group, GLT middle dose group, GLT high dose group, model group, sol- vent group （oil）, and positive group （JNJN）. Then the intragastric administration was used. After being treated with GLT for 60 days, the expression of Aβ1-40 in hippocampus was tested by immunohistochemistry. Results The ex- pression of Aβ1-40 in hippocampus increased in model rats, while GLT group significantly decreased. Conclusion GLT can protect AD model animals, and the following mechanisms may be decreasimz the deposition of Aβ.

关 键 词：灵芝三萜类化合物 阿尔茨海默病 自然衰老 Β-淀粉样肽 

分 类 号：R285.5[医药卫生—中药学]