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- Title
Restoration of hypertrophy-induced by norepinephrine through opening of ATP sensitive potassium channel.
- Authors
GUVEN, Celal; GUVEN, Eylem TASKIN; SEVGILER, Yusuf; OZALTUN, Betul; KOCAHAN, Sayad; SAHIN, Leyla
- Abstract
Norepinephrine (NE) has toxic effects on cardiomyocytes and induces myocardial hypertrophy, necrosis, progressive cardiac muscle damage via apoptosis. The hypertrophy has a beneficial effect on stressed-heart at early stage of it. But, it causes to increase some pathology, including heart failure or arrhythmia. ATP sensitive potassium channel (KATP) has been well documented to protect of cardiac tissue against some pathology including ischemia. The study aimed to evaluate the mechanism of protective effect of opening KATP in hypertrophic cardiomyocytes induced by norepinephrine. In the study, H9c2 cell line has used the research. It was created four groups as a control; hypertrophy; Diaxozide (Dia), one of KATP opener; Dia+hypertrophy. Distribution of actin filaments, mitochondrial membrane potential (MMP), and superoxide dismutase (SOD) enzyme activity was analyzed with proper tests, and then statistical analysis was performed. Although hypertrophy gave rise to decrease SOD enzyme activity, DIA co-treatment restored it. Hypertrophy destroyed cytoskeleton via actin distribution, but DIA ameliorated the distribution as well. Although hypertrophy caused to elevate MMP, DIA reversed its effect on MMP. Cardiomyocytes loss by oxidative stress-mediated apoptosis is an essential mechanism for norepinephrine-induced hypertrophy, and the alternations were attenuated with DIA cotreatment. Consequently, the opening of KATP has protective effects on NE-induced hypertrophy and DIA may be a candidate agent to protect the hypertrophic cell.
- Publication
Journal of Cellular Neuroscience & Oxidative Stress, 2018, Vol 10, Issue 2, p704
- ISSN
2149-7222
- Publication type
Academic Journal