{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T11:36:08Z","timestamp":1773920168166,"version":"3.50.1"},"reference-count":53,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T00:00:00Z","timestamp":1773878400000},"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. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Ulcerative colitis (UC) is a chronic and relapsing inflammatory bowel disease (IBD), that lacks specific therapeutic drugs. Prim-O-glucosylcimifugin (POG), a furanochromone glycoside derived from\n                      <jats:italic>Saposhnikovia divaricata<\/jats:italic>\n                      , exhibits anti-inflammatory, antioxidant, and anti-inflammasome activities. It has also been shown to inhibit the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. Given that ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal barrier dysfunction and NLRP3 activation, this study aims to investigate the therapeutic effects and underlying mechanisms of POG in a murine model of UC induced by dextran sulfate sodium (DSS), and to evaluate its potential translational significance for UC intervention.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A DSS-induced UC mouse model was employed to evaluate POG\u2019s therapeutic efficacy. Disease activity index, colon length, spleen index, and histopathological alterations of the colonic mucosa were assessed by H&amp;amp;E and AB-PAS staining, transmission electron microscopy, and immunofluorescence. Proinflammatory cytokines (TNF-\u03b1, IL-6, IL-18, IL-1\u03b2) were measured by ELISA, and NLRP3 inflammasome\u2013related proteins were analyzed by Western blot.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>POG treatment alleviated weight loss, colon shortening, splenomegaly, and inflammatory infiltration. It also restored goblet cell mucin droplets and tight junction proteins (Occludin, ZO-1, Claudin-1, MUC2), and reduced villi exfoliation. Serum levels of TNF-\u03b1, IL-6, IL-1\u03b2, and IL-18 were decreased. Western blot and ELISA revealed that POG suppressed NLRP3 inflammasome formation, inhibited GSDMD activation, and reduced cleavage and release of IL-1\u03b2 and IL-18. Collectively, these findings indicate that POG not only attenuates inflammatory injury but also protects epithelial barrier structure and function, supporting its potential value in mechanism-based UC therapy development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>POG ameliorates experimental UC by inhibiting NLRP3 inflammasome activation, thereby mitigating colonic inflammation, preserving mucosal barrier integrity, and blocking downstream inflammatory responses. POG shows promise as a therapeutic agent for UC and provides a rationale for further preclinical optimization and future clinical translation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1750305","type":"journal-article","created":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T06:47:59Z","timestamp":1773902879000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Prim-O-glucosylcimifugin ameliorates DSS-induced ulcerative colitis via suppressing NLRP3 inflammasome activation"],"prefix":"10.3389","volume":"17","author":[{"given":"Fuqian","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Xiong","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qingfeng","family":"Ruan","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chuanqi","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tingting","family":"Xie","sequence":"additional","affiliation":[{"name":"School of Foreign Languages, Hubei University of Chinese Medicine","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lu","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Wuhan No.1 Hospital","place":["Wuhan, China"]},{"name":"Department of Pharmacy, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,19]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1192","DOI":"10.1136\/gut.2009.197822","article-title":"Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome","volume":"59","author":"Bauer","year":"2010","journal-title":"Gut"},{"key":"B2","doi-asserted-by":"publisher","first-page":"2319","DOI":"10.1016\/j.celrep.2017.05.058","article-title":"Microbiota normalization reveals that canonical caspase-1 activation exacerbates chemically induced intestinal inflammation","volume":"19","author":"B\u0142a\u017cejewski","year":"2017","journal-title":"Cell. 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