Macrophage (M phi) phenotype and function play an important role in colonic inflammation, and Mf regulation contributes to healing colonic damage. To elucidate the role of macrophage and related mechanism in moxibustion action in ulcerative colitis (UC). UC model was established by supplying rats with drinking water containing 3.5% dextran sulfate sodium salt. High-temperature moxibustion (HM) at 43 +/- 1 degrees C was applied. Firstly, the colonic lesion was observed. Secondly, the functional phenotype and phagocytosis of peritoneal M phi (pM phi) were detected and differentiation of Mf due to the expression of specific cytokines were observed. UC model rats had a significantly larger number of CD11b(+)CD86(+) M phi in the abdominal cavity, with markedly more active phagocytosis and a significantly higher expression of inducible nitric oxide synthase (iNOs) mRNA compared to normal rats (all p < 0.05). They also showed apparent colonic damages. The abnormal expressions of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and migration inhibitory factor (MIF) were found. HM increased the number of CD11b(+)CD163(+) M phi in the peritoneal cavity and inhibited the phagocytic ability of pM phi, accompanied by high expressions of arginase I (Arg I) mRNA in pM phi and IL-4 and IL-13 in the abdominal cavity (all p < 0.05). HM encouraged the healing of colonic ulcers and alleviation of inflammation. Moxibustion promotes the healing of colonic injury and inflammation in UC rats, which is plausibly related to the thermal effect in modulating the activation of pM phi.