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Fig. 7 | Diabetology & Metabolic Syndrome

Fig. 7

From: 1α,25(OH)2D3 attenuates IL-6 and IL-1β-mediated inflammatory responses in macrophage conditioned medium-stimulated human white preadipocytes by modulating p44/42 MAPK and NF-κB signaling pathways

Fig. 7

1α,25(OH)2D3 attenuates Il-6 and IL-1β-mediated inflammatory responses in MacCM-stimulated human white preadipocytes. Accumulated macrophages infiltrating into white adipose tissue induce metaflammation, which is embodied by inflammatory responses including increased local gene expression and secretion of pro-inflammatory factors, particularly IL-1β, IL-6, IL-8, MCP-1 and RANTES. Among these pro-inflammatory factors, by binding to its receptor, IL-1β initiates and sustains the inflammatory responses in macrophage-stimulated preadipocytes by enhancing the phosphorylation of relA of the NF-κB signaling pathway, while in the same ligand-receptor manner IL-6 mediates similar responses by enhancing the phosphorylation of p44/42 MAPK. Besides directly inhibiting the pro-inflammatory gene expression (not tested in our study), 1α,25(OH)2D3 attenuates IL-1β-mediated inflammatory responses by decreasing the phosphorylation of relA in the nucleus. Moreover, 1α,25(OH)2D3 can exert a non-genomic action by decreasing the phosphorylation of p44/42 MAPK in the cytoplasm, to attenuate IL-6-mediated inflammatory responses

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Diabetology & Metabolic Syndrome

ISSN: 1758-5996

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