{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T08:16:52Z","timestamp":1778919412108,"version":"3.51.4"},"reference-count":33,"publisher":"Frontiers Media SA","issue":"6","license":[{"start":{"date-parts":[[2016,1,8]],"date-time":"2016-01-08T00:00:00Z","timestamp":1452211200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Exp Biol Med (Maywood)"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:p>Sufentanil, a commonly used opioid analgesic, could mimic ischemia postconditioning to attenuate ischemia reperfusion injury, but this effect might be hindered in diabetic animals by inhibition of glycogen synthase kinase-3\u03b2 phosphorylation. Also, diabetes can abrogate the cardioprotection of sevoflurane (an inhaled anesthetic) against ischemia reperfusion injury, and short-term insulin treatment does not restore protection by sevoflurane postconditioning. We hypothesized that long-term insulin treatment might restore the cardioprotective effect of sufentanil postconditioning in diabetic rats via phosphorylation of glycogen synthase kinase-3\u03b2. Streptozotocin (55\u2009mg\/kg)-induced diabetic rats received insulin (Novolin N, 6\u20138\u2009u\/d) for two days or two weeks, then were exposed to 30-min ischemia and 120-min reperfusion. Sufentanil postconditioning was performed 5\u2009min before the onset of reperfusion. Controls included non-diabetic rats, sham surgery for ischemia\/reperfusion, and sufentanil vehicle. Infarct size, cardiac troponin I, and phosphorylated glycogen synthase kinase-3\u03b2 were examined. Sufentanil postconditioning reduced infarct size by 46% in non-diabetic rats ( P\u2009&lt;\u20090.001), but diabetes prevented this protective effect. Two-day insulin treatment was not effective, but two-week treatment reduced infarct size by 45% ( P\u2009&lt;\u20090.001), reduced cardiac troponin I by 33% ( P\u2009&lt;\u20090.001), and increased phosphorylated glycogen synthase kinase-3\u03b2 levels ( P\u2009&lt;\u20090.001) in the diabetic sufentanil postconditioning group. In conclusion, sufentanil-induced cardioprotection was restored by long-term insulin treatment. The underlying mechanism may be increased phosphorylation of glycogen synthase kinase-3\u03b2.<\/jats:p>","DOI":"10.1177\/1535370215622706","type":"journal-article","created":{"date-parts":[[2016,1,9]],"date-time":"2016-01-09T20:07:39Z","timestamp":1452370059000},"page":"650-657","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Long-term insulin treatment restores cardioprotection induced by sufentanil postconditioning in diabetic rat heart"],"prefix":"10.3389","volume":"241","author":[{"given":"Yuwen","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei 230000, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei 230000, 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