The effect of Diazoxide on norepinephrine-induced cardiac hypertrophy, in vitro
Küçük Resim Yok
Tarih
2018
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Cellular and Molecular Biology Association
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Cardiac hypertrophy is associated with mitochondrial dysfunctions, which leads to heart failure if sustained. The aim of present study is to test hypothesis whether activation of mitochondrial KATP channel (mitoKATP) by diazoxide improve mitochondrial membrane potential (MMP) and oxidative stress in an in vitro model of cardiac hypertrophy. Rat cardiomyocytes cell line (H9c2) was used to create four groups as control, diazoxide, hypertrophy, hypertrophy and diazoxide. Norepinephrine was used to induce hypertrophy. Diazoxide and norepinephrine were simultaneously administered. After 24 hours treatment, total oxidant status (TOS), total antioxidant status (TAS) and superoxide dismutase (SOD) activities were measured. MMP and F-actin distribution were analyzed. Hypertrophy significantly elevated TOS level. In addition, diazoxide administration significantly increased TOS level in the normal cell line. There were no significant differences in SOD activity, TAS and oxidative stress index (OSI) between groups. Hypertrophy caused a decrease in MMP and destrupted F-actin. Diazoxide improved MMP and F-actin in mitochondria. Hypertrophy impaired the function and structure of mitochondria. The opening of mitoKATP by diazoxide failed to improve oxidative stress; however, it is effective against mitochondrial damage caused by hypertrophy. © 2018 by the C.M.B. Association.
Açıklama
Anahtar Kelimeler
Diazoxide, Hypertrophy, Membrane potential, Mitochondrial KATP channel, Oxidative stress
Kaynak
Cellular and Molecular Biology
WoS Q Değeri
Q4
Scopus Q Değeri
Q4
Cilt
64
Sayı
10
