학술논문
The pineal hormone melatonin attenuates doxorubicin induced-mitochondrial dysfunction and cardiotoxicity in vitro
Document Type
Journal Article
Source
Proceedings for Annual Meeting of The Japanese Pharmacological Society. 2018, :PO1-69
Subject
Language
English
ISSN
2435-4953
Abstract
Results: Isoproterenol-treatment increased peak OCR of H9c2 cells by ～30% which was inhibited by MEL [CON, 384±17; ISO, 496±33; ISO+MEL, 412±31 pmol/min; n=3 (six replicates); CON vs. ISO, p<0.05; ISO vs. ISO+MEL, p<0.05; CON vs. ISO+MEL, p>0.05]. Doxorubicin-treatment decreased OCR by ～40% which was reversed by MEL [CON, 934±69; DOX, 554±52; DOX+MEL, 858±97 pmol/min; n=3 (six replicates); CON vs. DOX, p<0.05; DOX vs. DOX+MEL, p<0.05; CON vs. DOX+MEL, p>0.05]. ISO and DOX significantly increased (～30%) and decreased (～25%) ECAR respectively (n=3, p<0.05) which was not inhibited by MEL. Melatonin alone had no significant effect on OCR and ECAR. Melatonin inhibited DOX-induced apoptosis in H9c2 cells [CON, 6.3±0.8%; DOX, 22±1.8%; DOX+MEL, 11±1.7%, n=4 (two replicates); CON vs. DOX, p<0.001; DOX vs. DOX+MEL, p<0.004; CON vs. DOX+MEL, p>0.05].