原儿茶酸对阿尔茨海默病模型小鼠体内多靶向的疗效及机制研究  

Study on Efficacy and Mechanism of Protocatechuic Acid in Multiple Target in Mice Model with Alzheimer’s Disease

作　　者：薛小燕[1] 巫莉萍[1] 王丽芳[1] XUE Xiao-yan;WU Li-ping;WANG Li-fang(The People’s Hospital of Ganzhou,Ganzhou Jiangxi 341000,China)

机构地区：[1]赣州市人民医院,江西赣州341000

出　　处：《抗感染药学》2020年第8期1090-1093,共4页Anti-infection Pharmacy

基　　金：江西省卫生计生委科技计划基金项目(编号:20174035)。

摘　　要：目的:研究原儿茶酸(PCA)对阿尔茨海默病(AD)模型小鼠体内多靶向治疗的疗效及机制。方法:采用D-半乳糖和三氯化铝(AlCl3)诱导AD动物模型,实验分为空白对照组、AD模型对照组、石杉碱甲组0.4 mg/(kg·d)以及PCA低剂量组5 mg/(kg·d)、PCA中剂量15 mg(kg·d)组和PCA高剂量30 mg/(kg·d)组,观察各剂量组小鼠Morris水迷宫逃避潜伏期的时间、原平台所在象限停留时间和病理变化,测定各组小鼠脑组织的AchE、Aβ、MAP、BDNF mRNA含量。结果:PCA低剂量组、PCA中剂量组小鼠的潜伏期时间短于AD模型(P<0.05),而其原平台所在象限停留时间均长于AD模型对照组(P<0.05);PCA各剂量组对AchE、Aβ和MAP mRNA表达量均低于AD模型对照组(P<0.05),且各组mRNA基本恢复正常水平;PCA各剂量组对BDNF mRNA表达量均高于AD模型对照组(P<0.05),且各组mRNA基本恢复正常水平。结论:PCA通过缩短潜伏期,延长原平台所在象限停留时间,降低AchE、Aβ和MAP mRNA表达水平,升高BDNF mRNA表达量等多靶向发挥神经营养作用。Objective:To study the efficacy and mechanism of protocatechuic acid(PCA)in multiple target in mice model with Alzheimer’s disease(AD).Methods:AD mice model was established by D-galactose(D-gal)and aluminum chloride(AlCl3).The experiment was divided into five groups:blank control group,AD model group,the therapeutic groups were administrated PCA respectively with low,medium,and high doses(5 mg·kg-1·d-1,15 mg·kg-1·d-1,30 mg·kg-1·d-1)through intragastric route for 5 weeks.Huperzine A(0.4 mg·kg-1·d-1)was used as a positive control drug.The test of Morris water-maze,the expression of AchE,Aβ,MAP and BDNF mRNA,immunohistochemical staining were carried out to evaluate the effects of PCA on the AD mice model.Results:Compared with AD model group,the mice administered by different doses of PCA had shorter escape latency and longer platform-crossing times except the group treated with higt dose PCA.Furthermore,PCA downregulated the expression of AchE,Aβand MAP mRNA,while upregulated the expression of BDNF.Conclusion:These findings provide the efficacy and mechanism of PCA in multiple target in mice model with Alzheimer’s disease through shortening escapelatency and extending platform-crossing times,downregulating the expression of AchE,Aβand MAP,while upregulating the expression of BDNF.

关 键 词：原儿茶酸 阿尔茨海默病 AD模型小鼠 体内疗效与机制 

分 类 号：R969[医药卫生—药理学]