Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/71770
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dc.contributor.authorKodchanan Singhanaten_US
dc.contributor.authorNattayaporn Apaijaien_US
dc.contributor.authorThidarat Jaiwongkamen_US
dc.contributor.authorSasiwan Kerdphooen_US
dc.contributor.authorSiriporn C. Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.date.accessioned2021-01-27T04:06:13Z-
dc.date.available2021-01-27T04:06:13Z-
dc.date.issued2020-01-01en_US
dc.identifier.issn20901232en_US
dc.identifier.other2-s2.0-85092206779en_US
dc.identifier.other10.1016/j.jare.2020.09.007en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85092206779&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/71770-
dc.description.abstract© 2020 Introduction: Previous studies reported the beneficial effects of pretreatment with melatonin on the heart during cardiac ischemia/reperfusion (I/R) injury. However, the effects of melatonin given after cardiac ischemia, as well as its comparative temporal effects are unknown. These include pretreatment, during ischemia, and at the onset of reperfusion. Also, the association between melatonin receptors and cardiac arrhythmias, mitochondrial function and dynamics, autophagy, and mitophagy during cardiac I/R have not been investigated. Objectives: We tested two major hypotheses in this study. Firstly, the temporal effect of melatonin administration exerts different cardioprotective efficacy during cardiac I/R. Secondly, melatonin provides cardioprotective effects via MT2 activation, leading to improvement in cardiac mitochondrial function and dynamics, reduced excessive mitophagy and autophagy, and decreased cardiac arrhythmias, resulting in improved LV function. Methods: Male rats were subjected to cardiac I/R, and divided into 4 intervention groups: vehicle, pretreatment with melatonin, melatonin given during ischemia, and melatonin given at the onset of reperfusion. In addition, either a non-specific melatonin receptor (MT) blocker or specific MT2 blocker was given to rats. Results: Treatment with melatonin at all time points alleviated cardiac I/R injury to a similar extent, quantified by reduction in infarct size, arrhythmia score, LV dysfunction, cardiac mitochondrial dysfunction, imbalance of mitochondrial dynamics, excessive mitophagy, and a decreased Bax/Bcl2 ratio. In H9C2 cells, melatonin increased %cell viability by reducing mitochondrial dynamic imbalance and a decrease in Bax protein expression. The cardioprotective effects of melatonin were dependent on MT2 activation. Conclusion: Melatonin given before or after ischemia exerted equal levels of cardioprotection on the heart with I/R injury, and its beneficial effects on cardiac arrhythmias, cardiac mitochondrial function and dynamics were dependent upon the activation of MT2.en_US
dc.subjectMultidisciplinaryen_US
dc.titleMelatonin as a therapy in cardiac ischemia-reperfusion injury: Potential mechanisms by which MT2 activation mediates cardioprotectionen_US
dc.typeJournalen_US
article.title.sourcetitleJournal of Advanced Researchen_US
article.stream.affiliationsChiang Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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