Sodium butyrate alleviates colitis by inhibiting mitochondrial ROS mediated macrophage pyroptosis.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro laboratory study without human subjects.
PubMed 40044062 · doi:10.1016/j.bbadis.2025.167756
What was done
Researchers evaluated the therapeutic effects and mechanisms of sodium butyrate (NaB) in experimental colitis. They administered oral NaB to a dextran sulfate sodium (DSS)-induced colitis rat model and analyzed serum and colonic inflammatory markers. Mechanistic investigations were performed in vitro using RAW264.7 macrophages stimulated with LPS and Nigericin to evaluate cytokine release, ERK and NF-κB signaling, mitochondrial ROS (Mito-ROS), mitochondrial membrane potential (JC-1), and pyroptosis. Effects on intestinal epithelial barrier integrity (ZO-1 and Occludin expression) were evaluated in CaCo2 cells.
What was found
The abstract reports directional findings without numerical values, effect sizes, or confidence intervals. Oral NaB prevented colitis and decreased serum and colonic inflammatory markers in DSS-treated rats. In vitro, NaB suppressed LPS-induced inflammatory cytokine production and inhibited ERK and NF-κB activation in RAW264.7 macrophages. NaB also attenuated LPS- and Nigericin-induced macrophage pyroptosis, restored mitochondrial membrane potential (JC-1), and decreased Mito-ROS production, leading to increased ZO-1 and Occludin tight junction protein expression in CaCo2 cells.
Why it matters
This study identifies inhibition of mitochondrial ROS-driven macrophage pyroptosis and preservation of epithelial barrier proteins as mechanisms by which butyrate suppresses colonic inflammation in preclinical models.
Limits
Findings are restricted to rodent and cell-culture models, which do not fully replicate human inflammatory bowel disease pathology. The abstract omits sample sizes (n), specific dosages, control details, and quantitative statistical metrics.
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