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Melatonin confers cardioprotective effect by suppressing oxidative damage. However, the effect and mechanism of melatonin on myocardial ischemia\u2013reperfusion (MI<\/jats:styled-content>\/R) injury in type 2 diabetic state are still unknown. In this study, we developed high\u2010fat diet\u2010fed streptozotocin (HFD<\/jats:styled-content>\u2010STZ<\/jats:styled-content>) rat, a well\u2010known type 2 diabetic model, to evaluate the effect of melatonin on MI<\/jats:styled-content>\/R injury with a focus on silent information regulator 1 (SIRT<\/jats:styled-content>1) signaling, oxidative stress, and PERK<\/jats:styled-content>\/eIF<\/jats:styled-content>2\u03b1<\/jats:italic>\/ATF<\/jats:styled-content>4\u2010mediated ER<\/jats:styled-content> stress. HFD<\/jats:styled-content>\u2010STZ<\/jats:styled-content> treated rats were exposed to melatonin treatment in the presence or the absence of sirtinol (a SIRT<\/jats:styled-content>1 inhibitor) and subjected to MI<\/jats:styled-content>\/R surgery. Compared with nondiabetic animals, type 2 diabetic rats exhibited significantly decreased myocardial SIRT<\/jats:styled-content>1 signaling, increased apoptosis, enhanced oxidative stress, and ER<\/jats:styled-content> stress. Additionally, further reduced SIRT<\/jats:styled-content>1 signaling, aggravated oxidative damage, and ER<\/jats:styled-content> stress were found in diabetic animals subjected to MI<\/jats:styled-content>\/R surgery. Melatonin markedly reduced MI<\/jats:styled-content>\/R injury by improving cardiac functional recovery and decreasing myocardial apoptosis in type 2 diabetic animals. Melatonin treatment up\u2010regulated SIRT<\/jats:styled-content>1 expression, reduced oxidative damage, and suppressed PERK<\/jats:styled-content>\/eIF<\/jats:styled-content>2\u03b1<\/jats:italic>\/ATF<\/jats:styled-content>4 signaling. However, these effects were all attenuated by SIRT<\/jats:styled-content>1 inhibition. Melatonin also protected high glucose\/high fat cultured H9C2 cardiomyocytes against simulated ischemia\u2013reperfusion injury\u2010induced ER<\/jats:styled-content> stress by activating SIRT<\/jats:styled-content>1 signaling while SIRT<\/jats:styled-content>1 siRNA<\/jats:styled-content> blunted this action. Taken together, our study demonstrates that reduced cardiac SIRT<\/jats:styled-content>1 signaling in type 2 diabetic state aggravates MI<\/jats:styled-content>\/R injury. Melatonin ameliorates reperfusion\u2010induced oxidative stress and ER<\/jats:styled-content> stress via activation of SIRT<\/jats:styled-content>1 signaling, thus reducing MI<\/jats:styled-content>\/R damage and improving cardiac function.<\/jats:p>","DOI":"10.1111\/jpi.12269","type":"journal-article","created":{"date-parts":[[2015,8,20]],"date-time":"2015-08-20T15:55:18Z","timestamp":1440086118000},"page":"376-390","source":"Crossref","is-referenced-by-count":103,"title":["Reduced silent information regulator 1 signaling exacerbates myocardial ischemia\u2013reperfusion injury in type 2 diabetic rats and the protective effect of melatonin"],"prefix":"10.1111","volume":"59","author":[{"given":"Liming","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Surgery Xijing Hospital The Fourth Military Medical University Xi'an 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