{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T16:59:22Z","timestamp":1785862762493,"version":"3.56.0"},"reference-count":36,"publisher":"Wiley","issue":"17","license":[{"start":{"date-parts":[[2020,8,11]],"date-time":"2020-08-11T00:00:00Z","timestamp":1597104000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Myocardial ischaemia\u2010reperfusion (I\/R) injury is a serious illness with high morbidity and mortality. Mounting evidence indicates the utility of sevoflurane (SEV) in the treatment of myocardial I\/R injury. This study aimed to explore the molecular mechanisms underlying the protective action of SEV against myocardial I\/R injury. A rat model of myocardial I\/R injury was established, and I\/R rats were treated with different concentrations of SEV. MicroRNA\u2010203 (miR\u2010203) and doublecortin (DCX) expression levels were determined using reverse transcription\u2010quantitative polymerase chain reaction. Putative target relationship between miR\u2010203 and DCX was explored using dual\u2010luciferase reporter gene assay and RNA\u2010binding protein immunoprecipitation assay. Ischaemia\u2010reperfusion rats were treated with SEV, miR\u2010203 antagomir or sh\u2010DCX, followed by determination of oxidative stress\u2010 and inflammation\u2010related factor levels using nitrite and enzyme\u2010linked immunosorbent assays, and that of apoptosis\u2010related factors using Western blot analysis. The apoptotic rate of myocardial tissues was determined using TdT\u2010mediated dUTP\u2010biotin nick end labeling (TUNEL) staining, and the infract area was evaluated using triphenyltetrazolium chloride staining. The results showed miR\u2010203 was poorly expressed and DCX was highly expressed in myocardial tissues of I\/R rats. Sevoflurane was found to elevate miR\u2010203, and miR\u2010203, in turn, could target and reduce DCX expression. Sevoflurane, miR\u2010203 overexpression or DCX silencing resulted in declined oxidative stress, inflammation, apoptosis and infarct area, ultimately alleviating myocardial I\/R injury. Collectively, these findings showed that SEV\u2010activated miR\u2010203 exhibited suppressive effects on myocardial I\/R injury in rats and highlighted the SEV\/miR\u2010203\/DCX axis as a promising therapeutic target for myocardial I\/R injury management.<\/jats:p>","DOI":"10.1111\/jcmm.15566","type":"journal-article","created":{"date-parts":[[2020,8,12]],"date-time":"2020-08-12T04:30:37Z","timestamp":1597206637000},"page":"9825-9838","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["MicroRNA\u2010203\u2013mediated inhibition of doublecortin underpins cardioprotection conferred by sevoflurane in rats after myocardial ischaemia\u2010reperfusion injury"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1834-3178","authenticated-orcid":false,"given":"Jian","family":"Tan","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Pingxiang People's Hospital of Southern Medical University Pingxiang P. 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