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Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy

  • Authors:
    • Junwang Du
    • Yan Zhou
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    Affiliations: Department of Anesthesiology, Tianshui First People's Hospital, Tianshui, Gansu 741000, P.R. China, Department of Critical Care Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510150, P.R. China
    Copyright: © Du et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 187
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    Published online on: March 14, 2023
       https://doi.org/10.3892/etm.2023.11886
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Abstract

Myocardial injury is an indicator of poor prognosis in sepsis, whereas propofol has been reported to protect the myocardium. Therefore, the present study investigated the effect of propofol on myocardial injury in sepsis and its mechanism. An in vitro model of myocardial cell injury was established in myocardial H9C2 cells using lipopolysaccharide (LPS). The Cell Counting Kit 8 (CCK8) assay was used to investigate the effect of propofol pretreatment on the viability of normal and LPS‑challenged H9C2 cells, whereas the lactate dehydrogenase (LDH) detection kit was used to measure the levels of LDH. The expression levels of LC3 were analyzed using an immunofluorescence assay. Western blotting was performed to analyze the expression levels of autophagy‑related proteins. Following treatment with the autophagy inhibitor 3‑methyladenine, CCK8 assay, TUNEL assay, western blotting, 2,7‑dichlorohydrofluorescein diacetate assay and ELISA were performed to investigate whether propofol exerted its effects on cell viability, apoptosis, oxidative stress and inflammation via autophagy. Moreover, to further explore the regulatory mechanism of propofol in myocardial injury, sirtuin 1 (SIRT1) was knocked down via transfection with small interfering RNA, and SIRT1 protein was inhibited via the addition of the SIRT1 inhibitor EX527. The present study demonstrated that propofol activated autophagy in LPS‑induced cardiomyocytes, and reversed the effects of LPS on viability, apoptosis, oxidative stress and the inflammatory response. Moreover, SIRT1 knockdown and inhibition decreased the activation of autophagy and the protective effect of propofol on LPS‑induced cardiomyocytes. In conclusion, propofol reduced LPS‑induced cardiomyocyte injury by activating SIRT1‑mediated autophagy.
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Copy and paste a formatted citation
Spandidos Publications style
Du J and Zhou Y: Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy. Exp Ther Med 25: 187, 2023.
APA
Du, J., & Zhou, Y. (2023). Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy. Experimental and Therapeutic Medicine, 25, 187. https://doi.org/10.3892/etm.2023.11886
MLA
Du, J., Zhou, Y."Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy". Experimental and Therapeutic Medicine 25.4 (2023): 187.
Chicago
Du, J., Zhou, Y."Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy". Experimental and Therapeutic Medicine 25, no. 4 (2023): 187. https://doi.org/10.3892/etm.2023.11886
Copy and paste a formatted citation
x
Spandidos Publications style
Du J and Zhou Y: Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy. Exp Ther Med 25: 187, 2023.
APA
Du, J., & Zhou, Y. (2023). Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy. Experimental and Therapeutic Medicine, 25, 187. https://doi.org/10.3892/etm.2023.11886
MLA
Du, J., Zhou, Y."Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy". Experimental and Therapeutic Medicine 25.4 (2023): 187.
Chicago
Du, J., Zhou, Y."Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy". Experimental and Therapeutic Medicine 25, no. 4 (2023): 187. https://doi.org/10.3892/etm.2023.11886
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