Open AccessPropofol Through Upregulating Caveolin-3 Attenuates Post-Hypoxic Mitochondrial Damage and Cell Death in H9C2 Cardiomyocytes During Hyperglycemia
Author(s) -
Fan Deng,
Shuang Wang,
Liangqing Zhang,
Xiang Xie,
Shuyun Cai,
Haobo Li,
Guiling Xie,
Huilai Miao,
Yang Chang-min,
Xin Liu,
Zhengyuan Xia
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000484680
Subject(s) - oxidative stress , viability assay , lactate dehydrogenase , apoptosis , creatine kinase , pharmacology , mitochondrion , cardioprotection , propofol , adenosine triphosphate , intracellular , chemistry , medicine , biology , endocrinology , ischemia , biochemistry , enzyme
Hearts from diabetic subjects are susceptible to myocardial ischemia reperfusion (I/R) injury. Propofol has been shown to protect against myocardial I/R injury due to its antioxidant properties while the underlying mechanism remained incompletely understood. Thus, this study aimed to determine whether or not propofol could attenuate myocardial I/R injury by attenuating mitochondrial dysfunction/damage through upregulating Caveolin (Cav)-3 under hyperglycemia.