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NLRP3 inflammasome activation plays an important role in myocardial ischemia\/reperfusion (MI\/R) injury. Our present study investigated whether diabetes aggravated MI\/R injury through NLRP3 inflammasome\u2010mediated pyroptosis. Type 1 diabetic rat model was established by intraperitoneal injection of streptozotocin (60\u2009mg\/kg). MI\/R was induced by ligating the left anterior descending artery (LAD) for 30\u2009minutes followed by 2\u2009h reperfusion. H9C2 cardiomyocytes were exposed to high glucose (HG, 30\u2009mM) conditions and hypoxia\/reoxygenation (H\/R) stimulation. The myocardial infarct size, CK\u2010MB, and LDH release in the diabetic rats subjected to MI\/R were significantly higher than those in the nondiabetic rats, accompanied with increased NLRP3 inflammasome activation and increased pyroptosis. Inhibition of inflammasome activation with BAY11\u20107082 significantly decreased the MI\/R injury. <jats:italic>In vitro<\/jats:italic> studies showed similar effects, as BAY11\u20107082 or the ROS scavenger N\u2010acetylcysteine, attenuated HG and H\/R\u2010induced H9C2 cell injury. In conclusion, hyperglycaemia\u2010induced NLRP3 inflammasome activation may be a ROS\u2010dependent process in pyroptotic cell death, and NLRP3 inflammasome\u2010induced pyroptosis aggravates MI\/R injury in diabetic rats.<\/jats:p>","DOI":"10.1155\/2017\/9743280","type":"journal-article","created":{"date-parts":[[2017,9,14]],"date-time":"2017-09-14T21:00:32Z","timestamp":1505422832000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":308,"title":["NLRP3 Inflammasome Activation\u2010Mediated Pyroptosis Aggravates Myocardial Ischemia\/Reperfusion Injury in Diabetic 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