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Involvement of TREK-1 Channel in Cell Viability of H9c2 Rat Cardiomyoblasts Affected by Bupivacaine and Lipid Emulsion

1
Departments of Medicine and Thoracic and Cardiovascular Surgery, College of Medicine, Gyeongsang National University, Jinju 52727, Korea
2
Gyeongsang National University Changwon Hospital, Changwon 51472, Korea
3
Department of Physiology, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Korea
4
Department of Convergence Medical Science, Gyeongsang National University, Jinju 52727, Korea
5
Department of Anesthesiology and Pain Medicine, College of Medicine, Gyeongsang National University, Jinju 52727, Korea
*
Authors to whom correspondence should be addressed.
Cells 2019, 8(5), 454; https://doi.org/10.3390/cells8050454
Received: 20 April 2019 / Revised: 13 May 2019 / Accepted: 14 May 2019 / Published: 14 May 2019
PDF [1776 KB, uploaded 14 May 2019]

Abstract

Lipid emulsion (LE) therapy has been used to reduce overdose of bupivacaine (BPV)-induced cardiotoxicity. The TWIK-related potassium channel-1 (TREK-1) is inhibited by BPV and activated by polyunsaturated fatty acids, which are the main component in LE. These pharmacological properties inspired us to investigate whether the TREK-1 channel is associated with cell viability of H9c2 cardiomyoblasts affected by BPV and LE. Consistent with previous studies, BPV-induced cell death was reduced by LE treatment. The reduction in the TREK-1 expression level by BPV was alleviated by LE. The BPV cytotoxicity highly decreased in TREK-1 overexpressed cells but was the opposite in TREK-1 knocked-down cells. TREK-1 channel activators and inhibitors increased and decreased cell viability, respectively. BPV-induced depolarization of the plasma and mitochondrial membrane potential and increase in intracellular Ca2+ level were blocked by LE treatment. BPV-induced depolarization of membrane potential was reduced in TREK-1 overexpressed cells, indicating that TREK-1 channels mediate setting the resting membrane potentials as a background K+ channel in H9c2 cells. These results show that TREK-1 activity is involved in the BPV cytotoxicity and the antagonistic effect of LE in H9c2 cells and suggest that TREK-1 could be a target for action of BPV and LE.
Keywords: bupivacaine; cardiomyoblast; lipid emulsion; membrane potential; TREK-1 bupivacaine; cardiomyoblast; lipid emulsion; membrane potential; TREK-1
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Yang, J.H.; Siregar, A.S.; Kim, E.-J.; Nyiramana, M.M.; Shin, E.-J.; Han, J.; Sohn, J.-T.; Kim, J.W.; Kang, D. Involvement of TREK-1 Channel in Cell Viability of H9c2 Rat Cardiomyoblasts Affected by Bupivacaine and Lipid Emulsion. Cells 2019, 8, 454.

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