丁酸盐在炎症反应中作用机制的研究进展  

Research progress on the mechanism of butyrate in inflammatory reaction

作　　者：张锦涛[1] 伊曼[1] 李志嘉[1] 孙素霞[1] 

机构地区：[1]南方医科大学公共卫生与热带医学学院营养与食品卫生学系,广州510515

出　　处：《免疫学杂志》2015年第12期1101-1104,共4页Immunological Journal

基　　金：国家自然科学基金(81202204);广东省自然科学基金(2012010009467);广东省大学生创新训练项目(201412121107);南方医科大学优秀青年教师项目;南方医科大学大学生创新训练项目(201512121259)

摘　　要：丁酸是由食物中的膳食纤维在肠道中被微生物发酵分解而成的一种短链脂肪酸。丁酸盐能够增强肠黏膜免疫屏障作用,从而阻止细菌及其代谢产物等进入血液引起炎症反应。丁酸钠是一种组蛋白去乙酰化酶抑制剂(histone deacetylase inhibitors,HDACi),可以促进调节性T细胞(regulatory T-cell,Treg细胞)的增殖活化,对机体免疫调节有着重要的作用。另外,丁酸盐能够通过调控G蛋白偶联受体(G protein-coupled receptors,GPRs)以及NF-κB、JAK/STAT等炎症相关通路的活性,减少促炎细胞因子的释放,抑制肠道的炎症反应,维持肠道免疫平衡。本文拟对丁酸盐在炎症反应中的作用机制进行概述,为炎症性疾病的预防提供理论依据。Butyric acid one of the short chain fatty acids in human body that mainly produced by anaerobic glycolysis in colon from un-digested carbohydrates. Butyrate can enhance the barrier function of intestinal mucosa to prevent the bacteria and their metabolites invade into the blood and cause inflammation reaction. Butyrate can act as an inhibitor of histone deacetylase to promote the proliferation and activation of regulatory T-cell, which contributes to the homeostasis of intestinal immune system. Butyrate can also reduce the generation of pro-inflammatory cytokines by acting on inflammation related pathways such as G protein-coupled receptors, NF-κB signal pathway and JAK/STAT signal pathway to reduce the inflammatory reaction and maintain the intestinal immune balance. This paper summarize the mechanism of the action of butyrate in the inflammatory response in order to provide the theoretical basis for the prevention of inflammatory disease.

关 键 词：丁酸盐 炎症 HDACI TREG细胞 肠黏膜屏障 

分 类 号：R363[医药卫生—病理学]