Moxifloxacin ameliorates clinical disease activity and histopathological changes of acetic acid-induced colitis model in rat possibly through its effect on proinflammatory mediators and oxidative stress

Background: Moxifloxacin (MFX), a fluoroquinolone antibiotic, was found in previous study to exert an anti-inflammatory effect including reduction of proinflammatory cytokine expression, the aim of this research was to investigate the potential anti-inflammatory effect of MFX on acetic acid (AA)-induced colitis model in rats. Methods: About 40 males of Wistar rats were divided into four groups as following, the negative (healthy) control group, AA-colitis group, sulfasalazine (SLS)group, and MFX group. Colitis induction was done by intra-rectal injection of 2 ml AA (4% v/v). After two hours of induction, SLS (100 mg/kg/day) and MFX (8 mg/kg/day) were given by oral route for seven consecutive days. Results: The administration of MFX substantially decreased the disease activity index (DAI), and histopathological alterations triggered by AA. Moreover, AA induced a significant rise in the production of the proinflammatory cytokine IL-1 beta, the adhesion molecules ICAM-1, and the oxidative stress (OS) biomarker myeloperoxidase (MPO) in colon homogenate. the MFX administration significantly reduced the production of proinflammatory cytokine IL-1 beta, adhesion molecules ICAM-1, and the OS biomarker myeloperoxidase (MPO) in colon homogenate, which were elevated by AA. The influences of MFX seemed comparable to those of SLS, with no significant difference between them. Conclusion: Consequently, MFX may possess a beneficial property in the treatment of ulcerative colitis (UC).