PINK1/Parkin pathway-mediated mitophagy by AS-IV to explore the molecular mechanism of muscle cell damage.
Astragaloside IV
Mitophagy
Myocyte injury
PINK1/Parkin pathway
Journal
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
ISSN: 1950-6007
Titre abrégé: Biomed Pharmacother
Pays: France
ID NLM: 8213295
Informations de publication
Date de publication:
May 2023
May 2023
Historique:
received:
17
01
2023
revised:
04
03
2023
accepted:
13
03
2023
medline:
3
4
2023
pubmed:
23
3
2023
entrez:
22
3
2023
Statut:
ppublish
Résumé
Functional disorders of mitochondria are closely related to muscle diseases. Many studies have also shown that oxidative stress can stimulate the production of a large number of reactive oxygen species (ROS), which have various adverse effects on mitochondria and can damage muscle cells. In this study, based on our previous research, we focused on the PINK1/Parkin pathway to explore the mechanism by which AS-IV alleviates muscle injury by inhibiting excessive mitophagy. L6 myoblasts were treated with AS-IV after stimulation with hydrogen peroxide (H After mitochondrial damage, the expression of malondialdehyde (MDA) and intracellular ROS in L6 myoblasts significantly increased, while the expression of superoxide dismutase (SOD) and ATP decreased. The mRNA and protein expression levels of Tom20 and Tim23 were decreased, while those of VDAC1 were increased. PINK1, Parkin, and LC3 II mRNA and protein expression increased, and P62 mRNA and protein expression decreased·H AS-IV is a potential drug for myasthenia gravis (MG), and its treatment mechanism is related to mediating mitophagy and restoring mitochondrial function through the PINK1/Parkin pathway.
Sections du résumé
BACKGROUND
BACKGROUND
Functional disorders of mitochondria are closely related to muscle diseases. Many studies have also shown that oxidative stress can stimulate the production of a large number of reactive oxygen species (ROS), which have various adverse effects on mitochondria and can damage muscle cells.
PURPOSE
OBJECTIVE
In this study, based on our previous research, we focused on the PINK1/Parkin pathway to explore the mechanism by which AS-IV alleviates muscle injury by inhibiting excessive mitophagy.
METHODS
METHODS
L6 myoblasts were treated with AS-IV after stimulation with hydrogen peroxide (H
RESULTS
RESULTS
After mitochondrial damage, the expression of malondialdehyde (MDA) and intracellular ROS in L6 myoblasts significantly increased, while the expression of superoxide dismutase (SOD) and ATP decreased. The mRNA and protein expression levels of Tom20 and Tim23 were decreased, while those of VDAC1 were increased. PINK1, Parkin, and LC3 II mRNA and protein expression increased, and P62 mRNA and protein expression decreased·H
CONCLUSION
CONCLUSIONS
AS-IV is a potential drug for myasthenia gravis (MG), and its treatment mechanism is related to mediating mitophagy and restoring mitochondrial function through the PINK1/Parkin pathway.
Identifiants
pubmed: 36948131
pii: S0753-3322(23)00321-9
doi: 10.1016/j.biopha.2023.114533
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
Carbonyl Cyanide m-Chlorophenyl Hydrazone
555-60-2
Hydrogen Peroxide
BBX060AN9V
Ubiquitin-Protein Ligases
EC 2.3.2.27
Protein Kinases
EC 2.7.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
114533Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of interest statement The authors declare that they have no conflict of interest regarding the publication of this article.