PMID- 38106638
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231219
IS  - 1687-8191 (Print)
IS  - 1687-8205 (Electronic)
IS  - 1687-8191 (Linking)
VI  - 2023
DP  - 2023
TI  - Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced 
      Cardiomyocytes Injury.
PG  - 2566754
LID - 10.1155/2023/2566754 [doi]
LID - 2566754
AB  - 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 mug/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.
CI  - Copyright (c) 2023 Yi-Mei Jin et al.
FAU - Jin, Yi-Mei
AU  - Jin YM
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Huang, Ai-Rong
AU  - Huang AR
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Yu, Mei-Qian
AU  - Yu MQ
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Ye, Wan-Ding
AU  - Ye WD
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Hu, Xiao-Guang
AU  - Hu XG
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Wang, Hua-Min
AU  - Wang HM
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Xu, Zhi-Wei
AU  - Xu ZW
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
FAU - Liang, Dong-Shi
AU  - Liang DS
AUID- ORCID: 0000-0002-5006-7508
AD  - Department of Pediatrics, Second Affiliated Hospital & Yuying Children's Hospital 
      of Wenzhou Medical University, Wenzhou 325027, China.
LA  - eng
PT  - Journal Article
DEP - 20231208
PL  - Egypt
TA  - J Toxicol
JT  - Journal of toxicology
JID - 101519097
PMC - PMC10723929
COIS- The authors declare that there are no conflicts of interest.
EDAT- 2023/12/18 06:41
MHDA- 2023/12/18 06:42
PMCR- 2023/12/08
CRDT- 2023/12/18 04:43
PHST- 2023/01/28 00:00 [received]
PHST- 2023/11/20 00:00 [revised]
PHST- 2023/11/27 00:00 [accepted]
PHST- 2023/12/18 06:42 [medline]
PHST- 2023/12/18 06:41 [pubmed]
PHST- 2023/12/18 04:43 [entrez]
PHST- 2023/12/08 00:00 [pmc-release]
AID - 10.1155/2023/2566754 [doi]
PST - epublish
SO  - J Toxicol. 2023 Dec 8;2023:2566754. doi: 10.1155/2023/2566754. eCollection 2023.