{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,27]],"date-time":"2026-06-27T22:45:52Z","timestamp":1782600352465,"version":"3.54.5"},"reference-count":40,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2018,4,17]],"date-time":"2018-04-17T00:00:00Z","timestamp":1523923200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100009331","name":"Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support","doi-asserted-by":"publisher","award":["ZYLX201703 to Y.B"],"award-info":[{"award-number":["ZYLX201703 to Y.B"]}],"id":[{"id":"10.13039\/501100009331","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>This study includes exploring (i) the production of endogenous hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) after mucosal wound generation and (ii) the role of compensating the change in H<jats:sub>2<\/jats:sub>S level postmucosal wound generation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and Materials<\/jats:title><jats:p>A mucosal wound model was established in female C57BL\/6J mice. Wound tissues were collected to examine the change in the endogenous H<jats:sub>2<\/jats:sub>S level. To examine the effect of decreased H<jats:sub>2<\/jats:sub>S, <jats:styled-content style=\"fixed-case\">GYY<\/jats:styled-content>4137 was intraperitoneally injected into mice at 50\u00a0mg\u00a0kg<jats:sup>\u22121<\/jats:sup>\u00a0day<jats:sup>\u22121<\/jats:sup> before mucosal wounding to compensate for the decreased endogenous H<jats:sub>2<\/jats:sub>S. Finally, we confirmed the role of <jats:styled-content style=\"fixed-case\">GYY<\/jats:styled-content>4137 in inhibiting the M1 phenotype macrophage activation induced by <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> in peritoneal macrophages and <jats:styled-content style=\"fixed-case\">RAW<\/jats:styled-content>264.7.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The production of endogenous H<jats:sub>2<\/jats:sub>S and the expression of cystathionine b\u2010synthase and cystathionine g\u2010lyase in vivo were reduced significantly in early stage after wound. <jats:styled-content style=\"fixed-case\">GYY<\/jats:styled-content>4137 significantly inhibited the activation of the M1 phenotype induced by mucosal wound inflammation in vivo and <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> in vitro. Finally, we confirmed that <jats:styled-content style=\"fixed-case\">GYY<\/jats:styled-content>4137 inhibited <jats:styled-content style=\"fixed-case\">iNOS<\/jats:styled-content> expression via the <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB signaling pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The exogenous H<jats:sub>2<\/jats:sub>S donor <jats:styled-content style=\"fixed-case\">GYY<\/jats:styled-content>4137 compensated for the reduced endogenous H<jats:sub>2<\/jats:sub>S postmucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H<jats:sub>2<\/jats:sub>S supplementation may aid in controlling inflammation associated with mucosal wounds.<\/jats:p><\/jats:sec>","DOI":"10.1111\/odi.12838","type":"journal-article","created":{"date-parts":[[2018,1,31]],"date-time":"2018-01-31T03:28:36Z","timestamp":1517369316000},"page":"793-801","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Exogenous hydrogen sulfide inhibits oral mucosal wound\u2010induced macrophage activation via the <scp>NF<\/scp>\u2010\u03baB pathway"],"prefix":"10.1111","volume":"24","author":[{"given":"R","family":"Zhuang","sequence":"first","affiliation":[{"name":"Department of Implant Dentistry Capital Medical University School of Stomatology  Beijing China"},{"name":"Laboratory of Tissue Regeneration and Immunology and Department of Periodontics Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Capital Medical University School of Stomatology  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Orthodontics Beijing Stomatological Hospital Capital Medical University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Du","sequence":"additional","affiliation":[{"name":"Laboratory of Tissue Regeneration and Immunology and Department of Periodontics Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Capital Medical University School of Stomatology  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7066-2654","authenticated-orcid":false,"given":"S","family":"Wang","sequence":"additional","affiliation":[{"name":"Molecular Laboratory for Gene Therapy and Tooth Regeneration Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Capital Medical University School of Stomatology  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