{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T01:33:43Z","timestamp":1790127223042,"version":"4.0.1"},"reference-count":40,"publisher":"Wiley","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"city government of Shenzhen, China","award":["17123915M"],"award-info":[{"award-number":["17123915M"]}]},{"name":"city government of Shenzhen, China","award":["17158616M"],"award-info":[{"award-number":["17158616M"]}]},{"name":"city government of Shenzhen, China","award":["17123915M"],"award-info":[{"award-number":["17123915M"]}]},{"name":"city government of Shenzhen, China","award":["17158616M"],"award-info":[{"award-number":["17158616M"]}]},{"name":"Research Grants Council of Hong Kong","award":["17123915M"],"award-info":[{"award-number":["17123915M"]}]},{"name":"Research Grants Council of Hong Kong","award":["17158616M"],"award-info":[{"award-number":["17158616M"]}]},{"name":"University of Hong Kong for Basic Science","award":["17123915M"],"award-info":[{"award-number":["17123915M"]}]},{"name":"University of Hong Kong for Basic Science","award":["17158616M"],"award-info":[{"award-number":["17158616M"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>. Excessive autophagy is a major mechanism of myocardial ischemia reperfusion injury (I\/RI) in diabetes with enhanced oxidative stress. Antioxidant N-acetylcysteine (NAC) reduces myocardial I\/RI. It is unknown if inhibition of autophagy may represent a mechanism whereby NAC confers cardioprotection in diabetes.<jats:italic> Methods and Results<\/jats:italic>. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5\u2009g\/kg\/day) for four weeks before being subjected to 30-minute coronary occlusion and 2-hour reperfusion. The results showed that cardiac levels of 15-F2t-Isoprostane were increased and that autophagy was evidenced as increases in ratio of LC3 II\/I and protein P62 and AMPK and mTOR expressions were significantly increased in diabetic compared to nondiabetic rats, concomitant with increased postischemic myocardial infarct size and CK-MB release but decreased Akt and eNOS activation. Diabetes was also associated with increased postischemic apoptotic cell death manifested as increases in TUNEL positive cells, cleaved-caspase-3, and ratio of Bax\/Bcl-2 protein expression. NAC significantly attenuated I\/RI-induced increases in oxidative stress and cardiac apoptosis, prevented postischemic autophagy formation in diabetes, and reduced postischemic myocardial infarction (all <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>p<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn fontstyle=\"italic\">0.05<\/mml:mn><\/mml:math>).<jats:italic> Conclusions<\/jats:italic>. NAC confers cardioprotection against diabetic heart I\/RI primarily through inhibiting excessive autophagy which might be a major mechanism why diabetic hearts are less tolerant to I\/RI.<\/jats:p>","DOI":"10.1155\/2017\/9257291","type":"journal-article","created":{"date-parts":[[2017,2,6]],"date-time":"2017-02-06T16:01:57Z","timestamp":1486396917000},"page":"1-10","source":"Crossref","is-referenced-by-count":50,"title":["N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy"],"prefix":"10.1155","volume":"2017","author":[{"given":"Sheng","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Science, Guangdong, 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