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

Area of Science:

• Gastroenterology
• Immunology
• Pharmacology

Background:

• Ulcerative colitis (UC) pathogenesis involves oxidative stress and cytokine signaling.
• Sodium butyrate (SB) exhibits antioxidant and anti-inflammatory properties, making it a potential therapeutic agent.

Purpose of the Study:

• To evaluate the efficacy of Sodium Butyrate (SB) in a dextran sulfate sodium (DSS)-induced mouse model of ulcerative colitis (UC).
• To assess SB's impact on oxidative stress markers, pro-inflammatory cytokines, and gut histology.

Main Methods:

• UC was induced in mice using DSS.
• Mice were treated with SB or 5-ASA (a standard treatment).
• Disease activity index (DAI), colon length, oxidative stress markers (MDA, MPO, SOD, GSH), and cytokine levels (TNF-α, IL-6) were measured.

Main Results:

• DSS administration significantly increased DAI, shortened colon length, elevated MDA, MPO, TNF-α, and IL-6, while decreasing SOD and GSH.
• SB treatment notably reduced DAI, preserved colon length, and modulated oxidative stress and cytokine levels.
• SB's therapeutic effects were comparable to 5-ASA, indicating significant anti-inflammatory and antioxidant activity.

Conclusions:

• Sodium butyrate (SB) effectively attenuated oxidative stress and pro-inflammatory responses in DSS-induced colitis.
• SB treatment restored redox balance and preserved mucosal architecture, suggesting its potential as a supplementary therapy for UC.
• SB demonstrates promise for managing ulcerative colitis by mitigating key pathological mechanisms.