@Article{biocell.2020.010323,
AUTHOR = {XINGXING ZHU, TIANFENG HUA, MINGFEI WU, JIATIAN WU, JIANCHAO HONG, MIN YANG},
TITLE = {Cardioprotective effect of ivabradine via the AMPK/SIRT1/PGC-1α signaling pathway in myocardial ischemia/reperfusion injury induced in H9c2 cell},
JOURNAL = {BIOCELL},
VOLUME = {44},
YEAR = {2020},
NUMBER = {3},
PAGES = {431--441},
URL = {http://www.techscience.com/biocell/v44n3/40243},
ISSN = {1667-5746},
ABSTRACT = {Post-resuscitation myocardial dysfunction (PRMD) is the most severe myocardial ischemia-reperfusion injury
(MIRI) and is characterized by difficult treatment and poor prognosis. Research has shown the protective effects of the
rational use of ivabradine (IVA) against PRMD; however, the molecular mechanisms of IVA remain unknown. In this
study, an ischemia-reperfusion injury (IRI) model was established using hypoxic chambers. The results demonstrated
that pretreatment with IVA reduced IRI-induced cytotoxicity and apoptosis. IVA attenuated mitochondrial damage,
eliminated excess reactive oxygen species (ROS), suppressed IRI-induced ATP and NAD<sup>+</sup>
, and increased the
AMP/ATP ratio. We further found that IVA increased the mRNA levels of sirtuin 1 (<i>SIRT1</i>) and peroxisome
proliferator-activated receptor-γ coactivator 1α (<i>PGC-1α</i>) and upregulated the expression levels of phosphorylated
AMP-activated protein kinase (p-AMPK)/AMPK, SIRT1, and PGC-1α proteins. Interestingly, no change in AMPK
mRNA levels was observed. Cardiomyocyte energy metabolism significantly changed after IRI. The aim of this study
was to demonstrate the cardioprotective effect of Ivabradine via the AMPK/SIRT1/PGC-1α signaling pathway in
myocardial ischemia/reperfusion injury-induced in H9c2 cell.},
DOI = {10.32604/biocell.2020.010323}
}