{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T10:34:08Z","timestamp":1790678048781,"version":"4.1.0"},"reference-count":32,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,6,12]],"date-time":"2019-06-12T00:00:00Z","timestamp":1560297600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Administration of propofol at the time of reperfusion has shown to protect the heart from ischemia and reperfusion (I\/R) injury. The aim of the present study was to investigate the molecular mechanism underling the cardioprotective effect of propofol against myocardial I\/R injury (MIRI) in vivo and in vitro. Rat heart I\/R injury was induced by ligation of the left anterior descending (LAD) artery for 30\u2009min followed by 2\u2010hr reperfusion. Propofol pretreatment (0.01\u2009mg\/g) was performed 10\u2009min before reperfusion. In vitro MIRI was investigated in cultured cardiomyocytes H9C2 following hypoxia\/reoxygenation (H\/R) injuries. Propofol pretreatment in vitro was achieved in the medium supplemented with 25\u2009\u03bcmol\/L propofol before H\/R injuries. Propofol pretreatment significantly increased miRNA\u2010451 expression, decreased HMGB1 expression, reduced infarct size, and I\/R\u2010induced cardiomyocyte apoptosis in rat hearts undergoing I\/R injuries. Knockdown of miRNA\u2010451 48\u2009hr before I\/R injury was found to increase HMGB1 expression, infarct size, and I\/R\u2010induced cardiomyocyte apoptosis in rat hearts in the presence of propofol pretreatment. These in vivo findings were reproduced in vivo that knockdown of miRNA\u2010451 48\u2009hr before H\/R injuries increased HMGB1 expression and H\/R\u2010induced apoptosis in cultured H9C2 supplemented with propofol. In addition, luciferase activity assays and gain\u2010of\u2010function studies found that propofol could decrease HMGB1, the target of miRNA\u2010541. Taken together our findings provide a first demonstration that propofol\u2010mediated cardioprotection against MIRI is dependent of microRNA\u2010451\/HMGB1. The study provides a novel target to prevent I\/R injury during propofol anesthesia.<\/jats:p>","DOI":"10.1002\/jcp.28897","type":"journal-article","created":{"date-parts":[[2019,6,12]],"date-time":"2019-06-12T12:36:40Z","timestamp":1560343000000},"page":"23289-23301","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Propofol\u2010mediated cardioprotection dependent of microRNA\u2010451\/HMGB1 against myocardial ischemia\u2010reperfusion injury"],"prefix":"10.1002","volume":"234","author":[{"given":"Yu\u2010mei","family":"Li","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Rizhao People's Hospital Rizhao Shandong Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin\u2010guo","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Rizhao Central Hospital Rizhao Shandong Province 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