{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T03:07:49Z","timestamp":1788318469538,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2017,4,7]],"date-time":"2017-04-07T00:00:00Z","timestamp":1491523200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2015A030313458"],"award-info":[{"award-number":["2015A030313458"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01HL116571"],"award-info":[{"award-number":["R01HL116571"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hydrogen sulphide (H<jats:sub>2<\/jats:sub>S) serves as a vital gastric mucosal defence under acid condition. Non\u2010steroidal anti\u2010inflammatory drugs (NSAIDs) are among widely prescribed medications with effects of antipyresis, analgesia and anti\u2010inflammation. However, their inappropriate use causes gastric lesions and endogenous H<jats:sub>2<\/jats:sub>S deficiency. In this work, we reported the roles of a novel pH\u2010controlled H<jats:sub>2<\/jats:sub>S donor (JK\u20101) in NSAID\u2010related gastric lesions. We found that JK\u20101 could release H<jats:sub>2<\/jats:sub>S under mild acidic pH and increase solution pH value. Intragastrical administration of aspirin (ASP), one of NSAIDs, to mice elicited significant gastric lesions, evidenced by mucosal festering and bleeding. It also led to infiltration of inflammatory cells and resultant releases of IL\u20106 and TNF\u2010\u03b1, as well as oxidative injury including myeloperoxidase (MPO) induction and GSH depletion. In addition, the ASP administration statistically inhibited H<jats:sub>2<\/jats:sub>S generation in gastric mucosa, while up\u2010regulated cyclooxygenase (COX)\u20102 and cystathionine gamma lyase (CSE) expression. Importantly, these adverse effects of ASP were prevented by the intragastrical pre\u2010administration of JK\u20101. However, JK\u20101 alone did not markedly alter the property of mouse stomachs. Furthermore, <jats:italic>in\u00a0vitro<\/jats:italic> cellular experiments showed the exposure of gastric mucosal epithelial (GES\u20101) cells to HClO, imitating MPO\u2010driven oxidative injury, decreased cell viability, increased apoptotic rate and damaged mitochondrial membrane potential, which were reversed by pre\u2010treatment with JK\u20101. In conclusion, JK\u20101 was proved to be an acid\u2010sensitive H<jats:sub>2<\/jats:sub>S donor and could attenuate ASP\u2010related gastric lesions through reconstruction of endogenous gastric defence. This work indicates the possible treatment of adverse effects of NSAIDs with pH\u2010controlled H<jats:sub>2<\/jats:sub>S donors in the future.<\/jats:p>","DOI":"10.1111\/jcmm.13166","type":"journal-article","created":{"date-parts":[[2017,4,7]],"date-time":"2017-04-07T10:18:42Z","timestamp":1491560322000},"page":"2441-2451","source":"Crossref","is-referenced-by-count":27,"title":["A novel pH\u2010controlled hydrogen sulfide donor protects gastric mucosa from aspirin\u2010induced injury"],"prefix":"10.1111","volume":"21","author":[{"given":"Chun\u2010tao","family":"Yang","sequence":"first","affiliation":[{"name":"Affiliated Cancer Hospital &amp; Institute Guangzhou Medical University Guangzhou China"},{"name":"Key Laboratory of Protein Modification and Degradation School of Basic Medical Sciences Guangzhou Medical University Guangzhou 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