Anti-macrophage Migration Inhibitory Factor Ameliorates Ulcerative Colitis In Mice And The Altered NF-?B And I?B Expression In Colon

Objective: To investigate the effect of anti-macrophage migration inhibitory factor monoclonal antibody(anti-MIF Ab)on dextran sulfate sodium(DSS)-induced colitis in mice.Furthermore,to investigate NF-?B p65?I?B? Expression in colon.Methods : Forty male BALB/c mice were randomly divided into normal group,UC model group,anti-MIF group intervention group and saline group.Normal group drinking distilled water for 7 days.The mice in UC model group,anti-MIF group intervention group and saline group drinking 5% dextran sulfate sodium(DSS)for 7 days to induced acute UC model.Those mice in anti-MIF group intervention group and saline group were given intraperitoneal injection of anti-MIF Ab and normal saline of 0.2mL at 1st?2nd?4th?6th day.To observe the protective effect of anti-MIF Ab in mice with ulcerative colitis,during modeling and the period of administration,Colitis was quantified by score disease activity and general situations index(DAI)of mice.After 8 days all mice were killed,the gross damage score in colon was performed,the colonic histopathological changes were observed under the light microscope on HE staining.NF-?Bp65 and I?B? expression in colon mucosa was further studied by immunohistochemistry.Results: Compared with normal control mice,The level of NF-?B p65 protein increased significantly in colon tissue of mice with UC,the level of I?B? slightly increased.After treatment with anti-MIF Ab,the expression level of NF-?B p65 significantly lower than that in UC model group,but the expression level of I?B? increased.Conclusions: These findings suggest that Anti-MIF monoclonal antibody have protective effect on intestinal mucosa of DSS-induced murine colitis.Anti-MIF monoclonal antibody reduced the expression of NF-?B p65 and increased the expression of I?B? in colonic mucosa of UC model mice.Our results therefore suggest that Anti-MIF monoclonal antibody inhibits the expression of inflammatory target genes downstream of NF-?B signaling pathway,Thus attenuating the inflammatory lesions of the UC model mouse colon mucosa.