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Purpose: To investigate the effect of thymol on dextran sulfate sodium (DSS)-induced experimental colitis in mice. Methods: Colitis in mice was induced by drinking water with 2.5 % (w/v) DSS. The levels of myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH) and superoxide (SOD) in colonic tissues were determined using commercial kits. Histological changes were evaluated by hematoxylin and eosin staining. The production of nitric oxide (NO) was measured by Griess assay. The levels of pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 were assessed by quantitative PCR and ELISA kits. Nuclear factor-kappaB (NF-κB) pathway activation was determined by Western blot. Results: Thymol markedly reduced disease activity index (DAI) scores, and recovered the colon length. Histological damage and MPO levels in the colonic tissues were markedly inhibited (p < 0.05) by thymol, which also reduced mRNA expressions of TNF-α, IL-1β and IL-6 in the colon. In addition, it downregulated MDA level but elevated GSH and SOD levels. Moreover, in vitro data showed that thymol significantly inhibited (p < 0.05) lipopolysaccharide-induced secretion of NO, TNF-α, IL-1β and IL-6 in macrophages, and suppressed (p < 0.05) the activation of NF-κB pathway. Conclusion: Thymol attenuates experimental colitis by down-regulating the activation of NF-κB pathway. Therefore, thymol is a potential candidate drug for the management of ulcerative colitis. Keywords: Thymol, Ulcerative colitis, Dextran sulfate sodium, Macrophages, Nuclear factor-kappaB

Thymol exerts anti-inflammatory effect in dextran sulfate sodium-induced experimental murine colitis