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-1β,
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 CD11b+F4/80+ and CD11b+F4/80+TIM-1+ and CD11b+F4/80+iNOS+ decreased significantly and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ increased significantly. Additionally,
curcumin significantly downregulated CD11b+F4/80+TLR4+ macrophages and the
protein levels of TLR2, TLR4, MyD88, NF-κBp65, 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.