Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11bF4/80 and CD11bF4/80TIM-1 and CD11bF4/80iNOS decreased significantly and CD11bF4/80CD206 and CD11bF4/80CD163 increased significantly. Additionally, curcumin significantly downregulated CD11bF4/80TLR4 macrophages and the protein levels of TLR2, TLR4, MyD88, NF-Bp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463179 | PMC |
http://dx.doi.org/10.1155/2021/3334994 | DOI Listing |
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