Frontiers in microbiology · 2026
Sodium acetate attenuates ulcerative colitis by reducing intestinal epithelial apoptosis and remodeling gut microbiota.
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Liu Qinxin, Han Rongshuang, Wang Yi, Mao Tao, Qi Xingsi, Cao Bin, Tian Zibin, Li Yukun
Аннотация
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 in vitro and in vivo. Cell viability was assessed using the CCK-8 assay. Colonic histopathology and mucus production were examined by H&E and AB/PAS staining. Immunohistochemistry, Western blotting, RT-qPCR, and ELISA were performed to detect barrier-related proteins, inflammatory cytokines, and apoptosis-associated molecules. Gut microbiota alterations were analyzed by 16S rRNA amplicon sequencing.
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-α, and IL-1β levels. Moreover, NaA inhibited excessive epithelial apoptosis. 16S rRNA amplicon sequencing and analysis showed that NaA partially reversed DSS-induced gut microbiota dysbiosis, as reflected by improved microbial diversity and community structure, increased Firmicutes/Bacteroidota ratio, reduced Bacteroides and Turicibacter abundance, and enrichment of potential beneficial genera, including Bifidobacterium, Lactobacillus, and Blautia.
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.
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 in vitro and in vivo. Cell viability was assessed using the CCK-8 assay. Colonic histopathology and mucus production were examined by H&E and AB/PAS staining. Immunohistochemistry, Western blotting, RT-qPCR, and ELISA were performed to detect barrier-related proteins, inflammatory cytokines, and apoptosis-associated molecules. Gut microbiota alterations were analyzed by 16S rRNA amplicon sequencing.
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-α, and IL-1β levels. Moreover, NaA inhibited excessive epithelial apoptosis. 16S rRNA amplicon sequencing and analysis showed that NaA partially reversed DSS-induced gut microbiota dysbiosis, as reflected by improved microbial diversity and community structure, increased Firmicutes/Bacteroidota ratio, reduced Bacteroides and Turicibacter abundance, and enrichment of potential beneficial genera, including Bifidobacterium, Lactobacillus, and Blautia.
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.