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| Lipid emulsion rescues bupivacaine-induced myocardial toxicity by activating autophagic flux |
| LIN Tingting, SHI Kejian, JIN Zhousheng, ZHANG Yujian, XIA Fangfang, LIU Le. |
| Department of Anesthesiology,the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China |
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| Cite this article: |
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LIN Tingting,SHI Kejian,JIN Zhousheng, et al. Lipid emulsion rescues bupivacaine-induced myocardial toxicity by activating autophagic flux[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(8): 609-614.
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Abstract Objective: To explore the role of autophagy in lipid emulsion to rescue myocardial toxicity of bupivacaine. Methods: The logarithmic growth of H9C2 cardiomyocytes were randomly divided into four groups: control group (DMSO group), bupivacaine group (Bup group), lipid emulsion group (Lip group), lipid emulsion+bupivacaine group (BLp group). After 24 hours of treatment with corresponding drugs, CCK8 was used to detect cell proliferation inhibition rate, cell morphology was observed under light microscope, cell autophagy was observed under electron microscope, and autophagy flow was detected under laser scanning confocal microscope. And we detected the expression of LC3II/I protein and p62 protein by Western blot and the expression of MAP1LC3 mRNA and p62 mRNA by RT-PCR in H9C2 cardiomyocytes. Results: Compared with the DMSO group, the Bup group significantly increased the myocardial cell proliferation inhibition rate (P<0.05),showed a large number of cell death and shrinkage, inhibited of autophagic flow, obviously increased of LC3II/I and p62 protein and mRNA expression (P<0.05). Compared with the Bup group, the BLp group and Lip group significantly reduced the myocardial cell proliferation inhibition rate (P<0.05), improved cardiomyocyte damage,promoted autophagic flow and accelerated the removal of autophagosomes, down regulated the expression of LC3II/I and p62 protein and mRNA (P<0.05). Conclusion: Lipid emulsion rescues bupivacaine-induced myocardial toxicity by activation autophagic flow, which accelerates the removal of autophagosomes.
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Received: 20 March 2021
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