Cardioprotective effects of melatonin against myocardial ischaemia/reperfusion injury: Activation of AMPK/Nrf2 pathway. Issue 13 (14th June 2021)

• Record Type: Journal Article
• Authors: Xu, Chennian; Wang, Jian; Fan, Zhenge; Zhang, Shuang; Qiao, Rui; Liu, Yu; Yang, Jian; Yang, Lifang; Wang, Huishan
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 13(2021)
• Page Start: 6455
• Page End: 6459
• Publication Date: 2021-06-14
• Subjects: AMPK/Nrf2 -- heart -- ischaemia/reperfusion injury -- melatonin -- oxidative stress; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16691
• Languages: English
• ISSNs: 1582-1838

Abstract

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.