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Article: N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy
Title | N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy |
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Authors | |
Issue Date | 2017 |
Publisher | Hindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/mi/index.html |
Citation | Mediators of Inflammation, 2017, v. 2017, p. 9257291 How to Cite? |
Abstract | Background. 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. Methods and Results. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5 g/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 p < 0.05). Conclusions. 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. |
Persistent Identifier | http://hdl.handle.net/10722/250168 |
ISSN | 2023 Impact Factor: 4.4 2023 SCImago Journal Rankings: 1.043 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wang, S | - |
dc.contributor.author | WANG, C | - |
dc.contributor.author | Yan, F | - |
dc.contributor.author | Wang, T | - |
dc.contributor.author | He, Y | - |
dc.contributor.author | Li, H | - |
dc.contributor.author | Xia, Z | - |
dc.contributor.author | Zhang, Z | - |
dc.date.accessioned | 2017-12-20T09:21:45Z | - |
dc.date.available | 2017-12-20T09:21:45Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Mediators of Inflammation, 2017, v. 2017, p. 9257291 | - |
dc.identifier.issn | 0962-9351 | - |
dc.identifier.uri | http://hdl.handle.net/10722/250168 | - |
dc.description.abstract | Background. 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. Methods and Results. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5 g/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 p < 0.05). Conclusions. 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. | - |
dc.language | eng | - |
dc.publisher | Hindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/mi/index.html | - |
dc.relation.ispartof | Mediators of Inflammation | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | N-Acetylcysteine Attenuates Diabetic Myocardial Ischemia Reperfusion Injury through Inhibiting Excessive Autophagy | - |
dc.type | Article | - |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | - |
dc.identifier.authority | Xia, Z=rp00532 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1155/2017/9257291 | - |
dc.identifier.scopus | eid_2-s2.0-85013392353 | - |
dc.identifier.hkuros | 283700 | - |
dc.identifier.volume | 2017 | - |
dc.identifier.spage | 9257291 | - |
dc.identifier.epage | 9257291 | - |
dc.identifier.isi | WOS:000394963100001 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0962-9351 | - |