TAILIEUCHUNG - Cobalt chloride alters mitochondrial function of in vitro cultured cardiomyocytes in a dose-dependent manner

This study was carried out to evaluate the effect of Cobalt chloride (CoCl2) on cardiac mitochondrial function in an in vitro model. In the study, H9C2 cardiomyocytes were cultured in a medium containing different concentrations of CoCl2. Cell viability, cardiolipin content, mitochondrial function, and mitochondrial oxidative stress were assessed by using Cell Counting Kit-8 and suitable fluorescence kits. | VNU Journal of Science Natural Sciences and Technology Vol. 37 No. 3 2021 44-49 Original Article Cobalt Chloride Alters Mitochondrial Function of In Vitro Cultured Cardiomyocytes in a Dose-dependent Manner Vu Thi Thu Pham Thi Bich VNU University of Science 334 Nguyen Trai Thanh Xuan Hanoi Vietnam Received 10 August 2021 Revised 19 August 2021 Accepted 31 August 2021 Abstract This study was carried out to evaluate the effect of Cobalt chloride CoCl2 on cardiac mitochondrial function in an in vitro model. In the study H9C2 cardiomyocytes were cultured in a medium containing different concentrations of CoCl2. Cell viability cardiolipin content mitochondrial function and mitochondrial oxidative stress were assessed by using Cell Counting Kit-8 and suitable fluorescence kits. The obtained data show that CoCl2 200 400 µM induced cell death and decreased mitochondrial function of H9C2 cardiomyocytes. Particularly CoCl2 at the dose of 300 µM significantly altered the values of mitochondrial membrane potential H2O2 - and O2 to and of 100 control respectively. Altogether CoCl2 strongly induced cardiomyocyte death via altering mitochondrial function in a dose-dependent manner. Keywords H9C2 mitochondria cell counting kit-8. 1. Introduction of hydroxylase enzymes is inhibited and HIF1α becomes stable 3 . Previous research shows Oxygen O2 -deficient environment plays a that Cobalt chloride CoCl2 has the ability to very important role in the pathological induce O deficiency by inhibiting hydroxylase conditions including myocardial ischemia 1 . activity and sustaining HIF1α 1 therefore Cells respond to the O2-deficiency conditions this compound has been widely used for by activating factor hypoxia inducing factor 1α establishing in vitro models of ischemic heart HIF1α a transcription factor regulating the disease. Mitochondria are intracellular expression of genes involved in cell survival respiratory organelles and strongly affected by .

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