Inhibition of excessive mitophagy by N-acetyl-L-tryptophan confers hepatoprotection against Ischemia-Reperfusion injury in rats.
H2O2
Hepatic ischemia-reperfusion injury
Mitophagy
N-acetyl-L-tryptophan
Journal
PeerJ
ISSN: 2167-8359
Titre abrégé: PeerJ
Pays: United States
ID NLM: 101603425
Informations de publication
Date de publication:
2020
2020
Historique:
received:
08
10
2019
accepted:
29
01
2020
entrez:
17
4
2020
pubmed:
17
4
2020
medline:
17
4
2020
Statut:
epublish
Résumé
In order to investigate the mechnism of hepatoprotective of N-acetyl-L-tryptophan (L-NAT) against ischemia-reperfusion (I/R) injury, the effects of L-NAT were investigated in hepatic ischemia-reperfusion injury (HIRI) models both in vitro and in vivo, which were made by BRL cells and Sprague-Dawley (SD) rats, respectively. The cell viability of hepatocyte was assessed by cell counting kit-8 (CCK-8) staining. The activation of autophagy was detected by electron microscopy (EM), quantitative real-time PCR (qRT-PCR), Western blotting and immunofluorescence. The activation of mitophagy was determined by the change of autophagy related protein, change of mitochondrial structure and function, co-location of autophagy protein and MitoTracker. Results showed that the morphological structures of hepatocytes were changed significantly after HIRI, and the cell viability of hydrogen peroxide (H
Identifiants
pubmed: 32296597
doi: 10.7717/peerj.8665
pii: 8665
pmc: PMC7151751
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e8665Informations de copyright
©2020 Li et al.
Déclaration de conflit d'intérêts
The authors declare there are no competing interests.
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