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Cardioprotective effects of melatonin against myocardial ischaemia/reperfusion injury: Activation of AMPK/Nrf2 pathway |
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| Authors: | Chennian Xu Jian Wang Zhenge Fan Shuang Zhang Rui Qiao Yu Liu Jian Yang Lifang Yang Huishan Wang |
| Affiliation: | 1. Department of Cardiovascular Surgery, General Hospital of Northern Theater Command, Shenyang, China;2. Department of Ultrasound, Chinese PLA 985 Hospital, Taiyuan, China Contribution: Data curation (equal), Formal analysis (equal), Writing - original draft (equal);3. Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi'an, China Contribution: Conceptualization (equal), Data curation (equal);4. Department of Anesthesiology, Xi'an Children's Hospital, Xi'an, China Contribution: Formal analysis (equal), Supervision (equal);5. Department of Cardiovascular Surgery, General Hospital of Northern Theater Command, Shenyang, China Contribution: Data curation (equal);6. Department of Cardiovascular Surgery, General Hospital of Northern Theater Command, Shenyang, China Contribution: Funding acquisition (equal);7. Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi'an, China;8. Department of Anesthesiology, Xi'an Children's Hospital, Xi'an, China |
| Abstract: | Although reperfusion is the most effective therapy for patients with acute myocardial infarction, reperfusion injury limits the therapeutic effects of early reperfusion. Oxidative stress plays a crucial role in myocardial ischaemia/reperfusion (I/R) injury. Melatonin, a circulating hormone, is well-known as an antioxidant in cardiovascular diseases. In this short communication, we show that melatonin significantly improves post-ischaemic cardiac function, reduces infarct size and decreases oxidative stress. Furthermore, melatonin markedly increases AMPK activation and Nrf2 nuclear translocation. Nevertheless, these melatonin-induced changes are abrogated by compound C. In addition, ML-385, an Nrf2 inhibitor, also withdraws the antioxidative effects of melatonin but has little effect on AMPK activation. In conclusion, our results demonstrate that melatonin alleviates myocardial I/R injury by inhibiting oxidative stress via the AMPK/Nrf2 signalling pathway. |
| Keywords: | AMPK/Nrf2 heart ischaemia/reperfusion injury melatonin oxidative stress |