MODULATING OXIDATIVE STRESS AND INFLAMMATION: SODIUM BUTYRATE'S THERAPEUTIC PROMISE IN EXPERIMENTAL COLITIS.

BACKGROUND

Oxidative stress and excessive cytokine signalling are central to the pathogenesis of ulcerative colitis (UC). Sodium butyrate (SB) has emerged as a potential therapeutic candidate due to its antioxidant and anti-inflammatory properties.

METHODS

UC was induced in Swiss albino mice using dextran sulfate sodium (DSS). Experiment groups included normal control (NC), DSS, DSS + SB, and DSS + 5-ASA. Clinical severity was assessed by the disease activity index (DAI) and colon length. Oxidative stress (MDA, MPO), antioxidants (SOD, GSH), Pro-inflammatory cytokines (TNF-α, IL-6), and histopathological scoring were assessed.

RESULTS

Increased DAI and shortening of the colon length with significantly elevated TNF-α and IL-6 levels and MDA and MPO, along with reduced GSH and SOD levels, which reflect oxidative damage and inflammation induced by DSS administration. Whereas treatment with SB therapy has been shown to lower DAI, preserve colon length, minimize MDA and MPO, restore GSH and SOD activity, and ameliorate cytokine levels, with effects comparable to those of 5ASA.

CONCLUSION

In DSS-induced colitis, the SB effectively attenuated oxidative stress and pro-inflammatory cytokine responses by restoring redox balance and preserving mucosal architecture. These findings suggest that administering SB as a supplementary treatment may be a viable option for managing UC.