α-Linolenic acid regulates macrophages via GPR120-NLRP3 inflammasome pathway to ameliorate diabetic rats

被引：11

作者：

Liu, Yuanyuan ^{[1
]}

Guo, Mixue ^{[1
]}

Li, Yiwei ^{[1
]}

Wang, Ting ^{[1
]}

Ren, Yi ^{[2
]}

Wang, Rui ^{[2
]}

Jiang, Xin ^{[2
]}

Zhang, Xiaoxia ^{[3
]}

Tian, Jianying ^{[1
]}

Wang, Hao ^{[1
]}

机构：

[1] Ningxia Med Univ, Sch Basic Med Sci, Key Lab Fertil Preservat & Maintainance, Minist Educ, Yinchuan, Peoples R China

[2] Ningxia Med Univ, Clin Med Coll, Yinchuan, Peoples R China

[3] Ningxia Med Univ, Coll Tradit Chinese Med, Yinchuan, Peoples R China

来源：

JOURNAL OF FUNCTIONAL FOODS | 2022年 / 99卷

基金：

中国国家自然科学基金;

关键词：

-Linolenic acid (ALA); Type 2 diabetes mellitus (T2DM); RAW264; 7; NLRP3; inflammasome; GPR120; INSULIN; OBESITY; ACTIVATION; MELLITUS; LINKS;

D O I：

10.1016/j.jff.2022.105348

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Type 2 diabetes mellitus (T2DM) is closely associated with chronic low-grade inflammation. Accumulating ev-idences suggest that GPR120 activation and NLRP3 inflammasome suppression contribute to ameliorate chronic inflammation. alpha-linolenic acid (ALA) has been proved to be beneficial in chronic metabolic diseases. However, the triggering mechanisms of ALA alleviated the inflammation in T2DM by GPR120-NLRP3 inflammasome pathway are still poorly understood. The present study was designed as two phase: in vivo, the levels of FBG, HbA1c, liver macrophages and NLRP3 inflammasome components were significantly attenuated with ALA intervention; in vitro, ALA inhibited the expression of NLRP3 inflammasome complex and the activation of NF-kappa B, enhanced GPR120 and subsequent beta-arrestin2 in LPS-stimulated RAW264.7 cells. Intriguingly, blocked with GPR120 antagonist AH7614, the inhibitory effects of ALA on NLRP3 inflammasome and TLR4/NF-kappa B pathway activity were weakened. Collectively, these results indicated that ALA regulated macrophages by GPR120-NLRP3 pathway to ameliorate T2DM.

引用

页数：11

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