Resveratrol improves CCL4-induced liver fibrosis in mouse by upregulating endogenous IL-10 to reprogramme macrophages phenotype from M(LPS) to M(IL-4)

Biomedicine & Pharmacotherapy

卷:117

Wei Luo¹  Hai-xing Jiang²  Shan-yu Qin³  Bang-li Hu³  Qing-yi Qin³  Bing Yu³ 

[1] Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China;

[2] Corresponding authors at: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, China.;

关键词: Resveratrol;    Liver fibrosis;    Macrophages phenotype;   

DOI  :  

来源: DOAJ

【 摘 要 】

Resveratrol has been suggested to mediate liver fibrosis. The switch from classically M(LPS) to alternatively activated M(IL-4) macrophages shows to protect organs from fibrosis. However, the mechanisms remain unclear. The study aimed to investigate whether resveratrol inhibited liver fibrosis by delivering IL-10 to promote the macrophage polarization in vitro and in vivo. We observed that resveratrol improved CCL4-induced liver fibrosis, upregulated Kupffer cells, increased the expression of IL-10 and M(IL-4) marks including Mrc1, Mrc2, CD163 and Arg1, whereas it slightly suppressed the level of M(LPS) including iNOS, TNF-α and MCP1. In vitro, resveratrol promoted the M(LPS) switch to M(IL-4) macrophage and elevated the expression of CD206 and iNOS as well. Meanwhile, IL-10 increased in both M(IL-4) and M(LPS). We concluded that resveratrol relieved liver fibrosis by producing more IL-10 to promote the polarization of M(LPS) to M(IL-4)-like macrophages.

【 授权许可】

Unknown