淫羊藿素对脂多糖诱导的阿尔茨海默病小鼠海马炎症反应的影响  

EFFECT OF ICARITIN ON LIPOPOLYSACCHARIDE-INDUCED INFLAMMATORY RESPONSE IN THE HIPPOCAMPUS OF MICE WITH ALZHEIMER’S DISEASE

作　　者：朱梦琳 王晓雯[1] 黄琳琳 郑欣慧 伏慧敏 陈文芳[1] ZHU Menglin;WANG Xiaowen;HUANG Linlin;ZHENG Xinhui;FU Huimin;CHEN Wenfang(Department of Physiology and Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao 266071, China)

机构地区：[1]青岛大学基础医学院生理学与病理生理学系

出　　处：《精准医学杂志》2019年第3期237-239,244,共4页Journal of Precision Medicine

基　　金：国家自然科学基金资助项目(31871144);青岛市科技局资助项目(18-6-1-76-nsh)

摘　　要：目的探讨淫羊藿素(ICT)对脂多糖(LPS)诱导的阿尔茨海默病(AD)模型小鼠海马炎症反应的影响及其机制。方法 ICR 小鼠20只,随机分为对照组(A组)、LPS组(B组)、LPS+ICT组(C组)、LPS+JB-1+ICT组(D组)。A组于侧脑室注射生理盐水;B组在侧脑室位注射LPS建立AD小鼠炎症模型;C组在LPS造模完成后连续12 d灌胃给予ICT;D组于ICT灌胃前1 h侧脑室给予胰岛素样生长因子-1受体(IGF-1R)的特异性阻断剂JB-1。采用Western Blot方法检测各组小鼠海马组织中诱导型一氧化氮合酶(iNOS)和环氧合酶(COX-2)蛋白的表达情况。结果 B组小鼠海马组织中iNOS和COX-2蛋白的表达与A组相比明显增加( F =7.156、8.172, q = 4.629、5.923, P <0.05);ICT可以明显抑制LPS对iNOS和COX-2蛋白表达的诱导作用( q =5.508、5.469, P <0.05);此作用可以被JB-1所阻断( q =4.425、3.599, P <0.05)。结论 ICT能够抑制LPS诱导 ICR 小鼠海马区的炎症反应,而IGF-1R信号通路可能参与了ICT的抗炎机制。Objective To investigate the effect of icaritin (ICT) on lipopolysaccharide (LPS)-induced inflammatory response in the hippocampus of mice model of Alzheimer’s disease (AD) and its mechanism. Methods Twenty ICR mice were randomly divided into control group (group A), LPS group (group B), LPS+ICT group (group C), and LPS+JB-1+ICT group (group D). Group A was injected with normal saline in the lateral ventricle;group B was injected with LPS in the lateral ventricle to establish an inflammation model in mice with AD;in group C, ICT was administered intragastrically for 12 consecutive days after LPS modeling was completed;group D was given an insulin-like growth factor-1 receptor (IGF-1R) specific blocker JB-1 in the lateral ventricle 1 h before intragastric administration of ICT. Western Blot was used to determine the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the hippocampal tissue of mice in each group. Results Group B showed significantly increased protein expression of iNOS and COX-2 in the hippocampal tissue compared with group A ( F =7.156,8.172;q =4.629,5.923;P <0.05). ICT significantly inhibited the protein expression of iNOS and COX-2 induced by LPS ( q =5.508,5.469;P <0.05), which could be blocked by JB-1 ( q =4.425,3.599;P <0.05). Conclusion ICT has an inhibitory effect on LPS-induced inflammatory response in the hippocampus of ICR mice, and the IGF-1R signaling pathway may be involved in the anti-inflammatory mechanism of ICT.

关 键 词：阿尔茨海默病 淫羊藿素 受体 IGF1型 脂多糖类 一氧化氮合酶 前列腺素内过氧化物合酶类 炎症 小鼠 近交 ICR 

分 类 号：R745.7[医药卫生—神经病学与精神病学]