Korean J Anesthesiol.
2023 Aug;76(4):368-382. 10.4097/kja.22572.
Lipid emulsion inhibits the cardiac toxicity caused by chloroquine via inhibition of reactive oxygen species production
- Affiliations
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- 1Department of Anesthesiology and Pain Medicine, Gyeongsang National University Changwon Hospital, Changwon, Korea
- 2Department of Anesthesiology and Pain Medicine, Gyeongsang National University College of Medicine, Jinju, Korea
- 3Institute of Medical Science, Gyeongsang National University, Jinju, Korea
- 4Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Jinju, Korea
- 5Division of Applied Life Science (BK21 Four), Gyeonsang National University, Jinju, Korea
- 6Department of Food Science and Technology, Institute of Agriculture and Life Science, Gyeongsang National University, Jinju, Korea
- 7Department of Anesthesiology and Pain Medicine, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju, Korea
- KMID: 2544556
- DOI: http://doi.org/10.4097/kja.22572
Abstract
- Background
Lipid emulsion (LE) is effective in treating intractable cardiac depression induced by the toxicity of highly lipid-soluble drugs including local anesthetics. However, the effect of LE on chloroquine (CQ)-evoked cardiac toxicity remains unclear. This study aimed to examine the effect of Lipofundin MCT/LCT, an LE, on the cardiotoxicity caused by CQ in H9c2 rat cardiomyoblasts and elucidate the underlying cellular mechanism.
Methods
The effects of CQ (1 × 10-4 M), LE, and the reactive oxygen species (ROS) scavengers mitotempo and N-acetyl-L-cysteine (NAC), alone or combined, on cell viability and migration, apoptosis, ROS production, calcium levels, mitochondrial membrane potential, and adenosine triphosphate (ATP) were examined. Additionally, the effects of LE on the activities of catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) induced by CQ were assessed.
Results
Pretreatment with LE, mitotempo, or NAC reversed the reduction in cell migration and viability, mitochondrial membrane potential, and ATP levels evoked by CQ, and inhibited the increase in cleaved caspase-3, ROS, and calcium concentration induced by CQ. LE inhibited the increase in Bax expression, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, MDA activity, and late apoptosis, and reversed the reduction in SOD and CAT activity induced by CQ. CQ did not significantly affect cleaved caspase-8 expression, and LE did not significantly affect CQ concentration.
Conclusions
Collectively, these results suggest that LE (Lipofundin MCT/LCT) inhibits the cardiotoxicity and late apoptosis induced by CQ toxicity via the intrinsic mitochondrial apoptotic pathway that is associated with direct inhibition of ROS production.
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