{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T16:46:10Z","timestamp":1787503570460,"version":"build-2736575974"},"reference-count":36,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2017,8,10]],"date-time":"2017-08-10T00:00:00Z","timestamp":1502323200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100012166","name":"National Basic Research Program of China","doi-asserted-by":"crossref","award":["2013CB945304"],"award-info":[{"award-number":["2013CB945304"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2017,9]]},"abstract":"Summary<\/jats:title>\n \n Acute myocardial ischaemia\/reperfusion (\n MIR<\/jats:styled-content>\n ) injury leads to severe arrhythmias and has a high rate of lethality. In the present study, we aim to determine the effect of dexmedetomidine (Dex) on heart injury parameters following\n MIR<\/jats:styled-content>\n surgery. We examined the effects of Dex on heart function parameters and infarct size following\n MIR<\/jats:styled-content>\n surgery. Proinflammatory cytokines, oxidative products and anti\u2010oxidative enzymes in the myocardium were measured to evaluate the anti\u2010inflammatory and anti\u2010oxidative effects of Dex. The role of the adenosine 5\u2032\u2010monophosphate (\n AMP<\/jats:styled-content>\n )\u2010activated protein kinase (\n AMPK<\/jats:styled-content>\n )\/phosphatidylino\u2010sitol 3\u2010kinase (\n PI<\/jats:styled-content>\n 3k)\/Akt\/endothelial nitric oxide synthase (\n eNOS<\/jats:styled-content>\n ) pathway was investigated using their inhibitors. The alteration of haemodynamic parameters, histopathological results, and infarct size caused by\n MIR<\/jats:styled-content>\n was attenuated by Dex. The interleukine\u20101 beta (\n IL<\/jats:styled-content>\n \u20101\u03b2),\n IL<\/jats:styled-content>\n \u20106, tumour necrosis factor\u2010a (\n TNF<\/jats:styled-content>\n \u2010\u03b1) and myeloperoxidase (\n MPO<\/jats:styled-content>\n ) were all significantly decreased. Anti\u2010oxidative enzymes superoxide dismutase (\n SOD<\/jats:styled-content>\n ), catalase and glutathione peroxidase (\n GP<\/jats:styled-content>\n x) were restored by Dex. Oxidative products8\u2010\n OH<\/jats:styled-content>\n dG,\n MDA<\/jats:styled-content>\n and protein carbonyl were all decreased by Dex (\n P<\/jats:italic>\n <.05). Dex activated\n AMPK<\/jats:styled-content>\n expression,\n eNOS<\/jats:styled-content>\n and Akt phosphorylation. The influence of Dex on cardiac function was reversed by the inhibitors of the\n eNOS<\/jats:styled-content>\n ,\n AMPK<\/jats:styled-content>\n and\n PI<\/jats:styled-content>\n 3K\/Akt pathways. These results indicate that Dex protected the cardiac functional, histological changes, inflammation and oxidative stress induced by\n MIR<\/jats:styled-content>\n . Our results present a novel signalling mechanism that Dex protects\n MIR<\/jats:styled-content>\n injury by activating an\n AMPK<\/jats:styled-content>\n \/\n PI<\/jats:styled-content>\n 3K\/Akt\/\n eNOS<\/jats:styled-content>\n pathway.\n <\/jats:p>","DOI":"10.1111\/1440-1681.12791","type":"journal-article","created":{"date-parts":[[2017,5,29]],"date-time":"2017-05-29T08:32:42Z","timestamp":1496046762000},"page":"946-953","source":"Crossref","is-referenced-by-count":51,"title":["Dexmedetomidine protects mice against myocardium ischaemic\/reperfusion injury by activating an AMPK\/PI3K\/Akt\/eNOS pathway"],"prefix":"10.1111","volume":"44","author":[{"given":"Yanjun","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Thoracic and Cardiovascular Surgery Shanghai Children's Medical Center Shanghai Jiaotong University School of Medicine Shanghai 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