Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced Cardiomyocytes Injury.

Autor: Jin YM; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Huang AR; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Yu MQ; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Ye WD; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Hu XG; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Wang HM; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Xu ZW; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China., Liang DS; Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Jazyk: angličtina
Zdroj: Journal of toxicology [J Toxicol] 2023 Dec 08; Vol. 2023, pp. 2566754. Date of Electronic Publication: 2023 Dec 08 (Print Publication: 2023).
DOI: 10.1155/2023/2566754
Abstrakt: Objective: The aim of this study was to investigate the effects of sodium hydrosulfide (NaHS) on Lipopolysaccharide (LPS)-induced cardiomyocyte injury in H9c2 cells.
Methods: H9c2 cardiomyocytes cultivated with medium containing 10  μ g/mL LPS were used to recapitulate the phenotypes of those in sepsis. Two sequential experiments were performed. The first contained a control group, a LPS group, and a LPS + NaHS group, with the aim to assure the protective effects of NaHS on LPS-treated cardiomyocytes. The second experiment added a fourth group, the LPS + NaHS + miR-133a-3p inhibition group, with the aim to preliminarily explore whether miR-133-3p exerts a protective function downstream of NaHS. The adenosine triphosphate (ATP) kit was used to detect ATP content; real-time quantitative polynucleotide chain reaction (qPCR) was used to measure the levels of mammalian targets of rapamycin (mTOR), AMP-dependent protein kinase (AMPK), and miR-133a-3p, and Western blot (WB) was used to detect protein levels of mTOR, AMPK, myosin-like Bcl2 interacting protein (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3I/II), and P62 (sequestosome-1, sqstm-1/P62).
Results: Compared with the control group, the expressions of miR-133a-3p ( P  < 0.001), P62 ( P  < 0.001), and the content of ATP ( P  < 0.001) decreased, while the expressions of Beclin-1 ( P  = 0.023) and LC3I/II ( P  = 0.048) increased in the LPS group. Compared with the LPS group, the expressions of miR-133a-3p ( P  < 0.001), P62 ( P  < 0.001), and the content of ATP ( P  < 0.001) in the NaHS + LPS group increased, while the expressions of Beclin-1 ( P  = 0.023) and LC3I/II ( P  = 0.022) decreased. Compared with the NaHS + LPS group, the expression levels of miR-133a-3p ( P  < 0.001), P62 ( P  = 0.001), and the content of ATP ( P  < 0.001) in the LPS + NaHS + miR-133a-3p inhibition group were downregulated, and the expression levels of Beclin-1 ( P  = 0.012) and LC3I/II ( P  = 0.010) were upregulated. The difference was statistically significant. There was no significant difference in the expression of AMPK and mTOR between groups.
Conclusion: Our research demonstrated that NaHS relieved LPS-induced myocardial injury in H9c2 by promoting the expression of miR-133a-3p, inhibiting autophagy in cardiomyocytes, and restoring cellular ATP levels.
Competing Interests: The authors declare that there are no conflicts of interest.
(Copyright © 2023 Yi-Mei Jin et al.)
Databáze: MEDLINE
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