Open AccessThe cystathionine γ-lyase/hydrogen sulfide pathway mediates the trimetazidine-induced protection of H9c2 cells against hypoxia/reoxygenation-induced apoptosis and oxidative stress
Author(s) -
Wenqing Zheng,
Chao Liu
Publication year - 2019
Publication title -
the anatolian journal of cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.364
H-Index - 28
eISSN - 2149-2271
pISSN - 2149-2263
DOI - 10.14744/anatoljcardiol.2019.83648
Subject(s) - trimetazidine , viability assay , cystathionine gamma lyase , oxidative stress , pharmacology , lactate dehydrogenase , cystathionine beta synthase , apoptosis , downregulation and upregulation , hypoxia (environmental) , cardioprotection , reactive oxygen species , medicine , chemistry , biochemistry , ischemia , enzyme , oxygen , cysteine , organic chemistry , gene
Trimetazidine is a piperazine-derived metabolic agent. It exerts cardioprotective effects against myocardial ischemia/reperfusion (I/R) injury. In addition, studies confirm that the cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway serves a beneficent role in attenuating myocardial I/R injury. However, the underlying role of the CSE/H2S pathway in the trimetazidine-induced protection against myocardial I/R injury remains elusive. Therefore, this study investigated whether trimetazidine ameliorates hypoxia/reoxygenation (H/R)-induced H9c2 cardiomyocyte injuries in an in vitro cell model of myocardial I/R injury, by enhancing the CSE/H2S pathway.