{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T06:24:02Z","timestamp":1787207042156,"version":"build-2736575974"},"reference-count":61,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T00:00:00Z","timestamp":1787184000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sodium acetate (NaA), an acetate donor among short-chain fatty acid salts, is involved in intestinal epithelial homeostasis, mucosal inflammation, and host\u2013microbiota 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      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\n                      <jats:italic>in vitro<\/jats:italic>\n                      and\n                      <jats:italic>in vivo<\/jats:italic>\n                      . Cell viability was assessed using the CCK-8 assay. Colonic histopathology and mucus production were examined by H&amp;amp;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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      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-\n                      <jats:italic>\u03b1<\/jats:italic>\n                      , and IL-1\u03b2 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\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      and\n                      <jats:italic>Turicibacter<\/jats:italic>\n                      abundance, and enrichment of potential beneficial genera, including\n                      <jats:italic>Bifidobacterium<\/jats:italic>\n                      ,\n                      <jats:italic>Lactobacillus<\/jats:italic>\n                      , and\n                      <jats:italic>Blautia<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fmicb.2026.1888741","type":"journal-article","created":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T05:29:09Z","timestamp":1787203749000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Sodium acetate attenuates ulcerative colitis by reducing intestinal epithelial apoptosis and remodeling gut microbiota"],"prefix":"10.3389","volume":"17","author":[{"given":"Qinxin","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rongshuang","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Mao","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingsi","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zibin","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yukun","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Hospital of Qingdao University","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,20]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"1602","DOI":"10.1053\/j.gastro.2021.12.288","article-title":"Pattern recognition receptor signaling and cytokine networks in microbial defenses and regulation of intestinal barriers: implications for inflammatory bowel disease","volume":"162","author":"Abraham","year":"2022","journal-title":"Gastroenterology"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"6119","DOI":"10.3390\/jcm14176119","article-title":"Emerging therapies in inflammatory bowel disease: a comprehensive review","volume":"14","author":"Appiah","year":"2025","journal-title":"J. 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