EGCG改善高果糖饮食小鼠代谢紊乱的作用与机制研究  

Regulatory Effect and Mechanism of EGCG on Metabolic Disorders in High-fructose Diet Mice

作　　者：周继红[1] 陈蔚[1] 丁乐佳 王岳飞[1] ZHOU Jihong;CHEN Wei;DING Lejia;WANG Yuefei(Tea Research Institute,Zhejiang University,Hangzhou 310058,China)

机构地区：[1]浙江大学茶叶研究所,浙江杭州310058

出　　处：《茶叶科学》2023年第3期399-410,共12页Journal of Tea Science

基　　金：国家自然科学基金区域创新联合基金(U19A2034)。

摘　　要：为探究表没食子儿茶素没食子酸酯(EGCG)对高果糖饮食诱导代谢紊乱的作用功效及机制,将15只雄性SPF级C57BL/6小鼠随机分为3组:正常饮食组(NCD)、高果糖饮食组(HFD)和高果糖补充1%EGCG饮食组(HFE)。饲喂8周后测定小鼠的体质量、能量利用率、ALT和AST含量及组织形态学染色等参数。ELISA检测肝脏TNF-α、IL-1β、IL-6和肠道IL-6炎症因子水平,实时荧光定量PCR检测肝脏Srebp-1c、Tlr4、Myd88及肠道Zo-1、Tlr4、Myd88基因表达水平,免疫组化检测ZO-1、Occludin蛋白表达水平。试验表明,膳食补充EGCG能够有效抑制高果糖饮食诱导的小鼠体重增加、脂肪积累、肝脏及肠道炎症因子释放,并可上调肠壁完整性相关的Zo-1基因表达水平和ZO-1、Occludin蛋白表达水平,下调肝脏中脂质代谢相关的Srebp-1c基因表达水平,下调肠道和肝脏中炎症相关的Tlr4、Myd88基因表达水平。以上结果表明,膳食补充EGCG对高果糖饮食诱导的代谢障碍和炎症反应有一定的预防作用,其机理可能与TLR4/MyD88信号通路介导的肠-肝轴调控机制有关。This study investigated the effects and mechanisms of epigallocatechin gallate (EGCG) on high-fructose diet-induced metabolic disorders.Fifteen male SPF C57BL/6 mice were randomly divided into three groups:normal diet group (NCD),high-fructose diet group (HFD),and high-fructose diet supplemented with 1%EGCG group(HFE),with 5 mice in each group.After 8 weeks of feeding,the body weight,energy utilization rate,ALT and AST levels,as well as tissue morphology staining of the mice were measured.Furthermore,hepatic TNF-α,IL-1β,IL-6and intestinal IL-6 inflammatory cytokine levels were detected by ELISA.The expressions of Srebp-1c,Tlr4,Myd88in liver and Zo-1,Occludin,Tlr4 and Myd88 in intestine were measured by quantitative real-time PCR.Protein expressions of ZO-1 and Occludin were detected by IHC.The results show that dietary supplementation of EGCG could effectively reduce high-fructose diet-induced body weight gain,fat accumulation,hepatic and intestinal inflammatory responses,and could improve the intestinal barrier function by upregulating the expression of Zo-1 and the protein expressions of ZO-1 and Occludin.It also modulated lipid metabolism by reducing the expression level of Srebp-1c in liver,and downregulated the expression levels of inflammatory-related genes (Tlr4 and Myd88) in colon and liver.The results above suggest that dietary supplementation of EGCG has a preventive effect on high-fructose diet-induced metabolic disorders and inflammatory responses,and its mechanism may be related to the regulation of the gut-liver axis mediated by the TLR4/MyD88 signaling pathway.

关 键 词：茶多酚 食源性肥胖 炎症反应 脂质代谢 肠-肝轴 

分 类 号：S571.1[农业科学—茶叶生产加工] R151.3[农业科学—作物学]