{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T18:16:57Z","timestamp":1780078617624,"version":"3.54.0"},"reference-count":27,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2017,7,17]],"date-time":"2017-07-17T00:00:00Z","timestamp":1500249600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004602","name":"Program for New Century Excellent Talents in University","doi-asserted-by":"publisher","award":["NCET\u201011\u20100870"],"award-info":[{"award-number":["NCET\u201011\u20100870"]}],"id":[{"id":"10.13039\/501100004602","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Nitric oxide is a potent anti\u2010apoptotic and cardioprotective molecule in healthy animals. However, recent study demonstrates that overexpression of <jats:styled-content style=\"fixed-case\">eNOS<\/jats:styled-content> exacerbates the liver injury in diabetic animals. whether diabetes may also alter <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>'s biologic activity in ischaemic\/reperfused heart remains unknown. The present experiment was designed to determine whether the nitric oxide donor, S\u2010nitrosoglutathione, may exert different effects on diabetic and non\u2010diabetic myocardial ischaemia\/reperfusion (<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\/R) injury. Diabetic state was induced in mice by multiple intraperitoneal injections of low\u2010dose streptozotocin (<jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>). The control or diabetic mice were subjected to 30\u00a0minutes ischaemia and 3 or 24\u00a0hours reperfusion. At 10\u00a0minutes before reperfusion, diabetic and non\u2010diabetic mice were received an intraperitoneal injection of S\u2010nitrosoglutathione (<jats:styled-content style=\"fixed-case\">GSNO<\/jats:styled-content>, a nitric oxide donor, 1\u00a0\u03bcmol\/kg). <jats:styled-content style=\"fixed-case\">GSNO<\/jats:styled-content> attenuated <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\/R injury in non\u2010diabetic mice, as measured by improved cardiac function, reduced infarct size and decreased cardiomyocyte apoptosis. In contrast, <jats:styled-content style=\"fixed-case\">GSNO<\/jats:styled-content> failed to attenuate but, rather, aggravated the <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\/R injury in diabetic mice. Mechanically, the diabetic heart exhibited an increased nitrative\/oxidative stress level, as measured by peroxynitrite formation, compared with non\u2010diabetic mice. Co\u2010administration of <jats:styled-content style=\"fixed-case\">GSNO<\/jats:styled-content> with <jats:styled-content style=\"fixed-case\">EUK<\/jats:styled-content>134 (a peroxynitrite scavenger) or Mn<jats:styled-content style=\"fixed-case\">TE<\/jats:styled-content>\u20102\u2010PyP5 (a superoxide dismutase mimetic) or Apocynin (a <jats:styled-content style=\"fixed-case\">NADPH<\/jats:styled-content> oxidase inhibitor) 10\u00a0minutes before reperfusion significantly decreased the <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\/R\u2010induced peroxynitrite formation and the <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\/R injury. Collectively, the present study for the first time demonstrated that diabetes may cause superoxide overproduction, increase <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> inactivation and peroxynitrite formation, and thus convert <jats:styled-content style=\"fixed-case\">GSNO<\/jats:styled-content> from a cardioprotective molecule to a cardiotoxic molecule.<\/jats:p>","DOI":"10.1111\/1440-1681.12781","type":"journal-article","created":{"date-parts":[[2017,5,13]],"date-time":"2017-05-13T14:26:37Z","timestamp":1494685597000},"page":"854-861","source":"Crossref","is-referenced-by-count":12,"title":["The opposite effects of nitric oxide donor, S\u2010nitrosoglutathione, on myocardial ischaemia\/reperfusion injury in diabetic and non\u2010diabetic mice"],"prefix":"10.1111","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0216-9200","authenticated-orcid":false,"given":"Yi","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology 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