ArticleCells2025
Lipid Emulsion Mitigates the Cardiotoxic Effects of Labetalol in Rat Cardiomyoblasts.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Preclinical Evaluation of Labetalol for Cutaneous Melanoma Drug Repurposing: Cytotoxic Activity in A375 Cells and Mitochondria-Associated Apoptotic Signaling.Medicina (Kaunas, Lithuania) · 2026Article
- Cytoprotective Effects of Lipid Emulsion Against Bupivacaine-Induced Cytotoxicity in Human Rotator Cuff Fibroblasts.Antioxidants (Basel, Switzerland) · 2026Article
- Enzymatic aminolysis in continuous flow: an efficient strategy for the synthesis of salicylamide derivatives.RSC advances · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Lipid emulsion has recently emerged as an effective agent for improving the cardiotoxicity of highly lipophilic drugs. However, its effect on cardiotoxicity induced by labetalol, a nonselective beta-blocker, remains unknown. In this study, we investigated the effects of lipid emulsion on the cardiotoxicity of labetalol in rat cardiomyoblasts and tried to decipher the underlying mechanisms. The effects of lipid emulsion on labetalol-induced changes in cell viability, expression of Bax/Bcl-2, cleaved caspase-3, and cleaved caspase-9, and phosphorylation of GSK-3β, Akt, and PI3K were examined. Lipid emulsion inhibited labetalol-induced decrease in cell viability, whereas LY294002, MK2206, and SB216763, the inhibitors of phosphoinositide 3-kinase (PI3K), Akt, glycogen synthase kinase-3β (GSK-3β), respectively, partially attenuated this restoration of cell viability. Lipid emulsion reversed the increase in expression of cleaved caspase-3, cleaved caspase-9, and Bax/Bcl-2 and decrease in the phosphorylation of GSK-3β, Akt, and PI3K by labetalol. Lipid emulsion and cyclosporin, a mitochondrial permeability transition pore (MPTP) inhibitor, reduced the labetalol-induced increase in the number of TUNEL-positive cells and promoted late-stage apoptosis. Overall, lipid emulsion inhibited apoptotic cell death caused by labetalol toxicity via the inhibition of intrinsic apoptotic pathway and MPTP in rat cardiomyoblasts, which appears to involve PI3K, Akt, and GSK-3β signaling pathways.
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