Objective: To elucidate if Emodin is participated in adipose tissue inflammation and its underlying mechanisms. Mmedia and violenceethods: 3T3-L1 adipocytes and RAW264.7 macrophages were co-cultured to mimic adipose tissue inflammation microenvironment in obesity in vitro. Real-time PCR and enzyme-linked immunosorbent assay(ELISA) were applied to examine the levels of IL-1β, IL-6, TNFα and Adiponectin in co-cultured cells and supernatants. Real-time PCR and western blot were performed to detect the expression of M1/M2 marker genes in CD11b microbeads isolated macrophages. Western blot was applied to detect JAK1 and STAT购买Dibutyryl-cAMP6 expression. Transwell migration assay was applied to determine the capacity of macrophage migration. STAT6 specific inhibitor AS1517499 was applied to elucidate the molecular mechanisms by which Emodin affects adipose tissue inflammation. Results: Emodin remarkably inhibited IL-1β, IL-6 and TNFα levels, whereas enhanced Adiponectin level in co-cultured cells and supernatants. Emodin apparently suppressed the expression of M1 marker gene(iNOS), whereas elevated the expression of M2 marker genes(IL-10 and Arg1) in isolated macrophages. Emodin greatly enhanced phosphorylated JAK1 and STAT6 levels. AS1517499 significantly abrogated the inhibitory effect of Emodin on the expression of inflammatory factors. Emodin remarkably repressed macrophage migration induced by adipocyte-conditioned medium. Conclusion: Emodin may decrease adipose tissue inflammation through promoting M2 macrophage polarization via JAK1/STAT6 signaling pathwawww.selleck.cn/products/Nolvadexy.