Lipoxin A4 attenuated dexamethasone-induced muscle atrophy via activation of PGC-1a/Nrf2/TFAM pathway
J. physiol. biochem
; 79(1): 107-115, feb. 2023. graf, ilus
Article
in English
| IBECS
| ID: ibc-215717
Responsible library:
ES1.1
Localization: ES15.1 - BNCS
ABSTRACT
Prolonged dexamethasone (DEX) administration causes skeletal muscle atrophy through induction of both oxidative stress and mitochondrial dysfunction. Lipoxin A4 (LXA4) is a recognized antioxidant but its effect against DEX-induced muscle atrophy has not been studied yet. This study aimed to assess the potential ameliorating effect of LXA4 on DEX-induced muscle atrophy and investigate the possible involvement of the mitochondrial dynamics pathway and the redox state in this effect. Forty male rats were divided into four groups; normal control, LXA4-treated, DEX-treated, and LXA4 plus DEX-treated. At the end of the experiment, LXA4 counteracted the effect of DEX on different parameters including muscle weight, muscle strength, serum creatine kinase activity, malondialdehyde and protein carbonyl contents, Na/K-ATPase and citrate synthase activities, mitochondrial transmembrane potential, mitochondrial transcription factor (TFAM), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and nuclear factor erythroid 2-related factor 2 (Nrf2). These findings signify the promising therapeutic effect of LXA4 against DEX-induced skeletal muscle atrophy and indicate the possible involvement of LXA4-induced mitochondrial activation in addition to its well-known antioxidant effects. (AU)
Full text:
Available
Collection:
National databases
/
Spain
Database:
IBECS
Main subject:
Muscular Atrophy
/
NF-E2-Related Factor 2
Limits:
Animals
Language:
English
Journal:
J. physiol. biochem
Year:
2023
Document type:
Article
Institution/Affiliation country:
Tanta University/Egypt