ArticleFrontiers in microbiology2026
Sodium acetate attenuates ulcerative colitis by reducing intestinal epithelial apoptosis and remodeling gut microbiota.
Article in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Sodium acetate (NaA), an acetate donor among short-chain fatty acid salts, is involved in intestinal epithelial homeostasis, mucosal inflammation, and host-microbiota interactions. However, its role in ulcerative colitis (UC), particularly in regulating epithelial apoptosis and gut microbiota remodeling, remains unclear. This study investigated the protective effects and potential mechanisms of NaA in experimental colitis. Methods: LPS-induced intestinal epithelial cell injury models using NCM460 and Caco-2 cells, together with a DSS-induced mouse colitis model, were established to evaluate the effects of NaA Results: NaA showed no obvious cytotoxicity within an appropriate concentration range and increased ZO-1 and Occludin expression in intestinal epithelial cells. Under LPS stimulation, NaA restored barrier protein expression and reduced the BAX/BCL-2 ratio and cleaved-caspase-3 expression in both NCM460 and Caco-2 cells. In DSS-induced colitis mice, NaA alleviated body weight loss, disease activity index elevation, colon shortening, and spleen index increase. NaA also attenuated colonic histological injury, increased AB/PAS-positive areas, restored ZO-1, Occludin, and MUC2 expression, and reduced IL-6, TNF- Conclusion: NaA alleviates experimental colitis by suppressing inflammation, inhibiting excessive epithelial apoptosis, preserving epithelial tight-junction and mucus barrier integrity, and partially restoring gut microbiota homeostasis. These findings suggest that acetate-based intervention may be a potential strategy for UC management through coordinated regulation of epithelial protection and microbial remodeling.
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