DHEA Alleviates Oxidative Stress of Muscle Cells via Activation of Nrf2 Pathway

Dehydroepiandrosterone (DHEA) has been proposed to regulate muscle dystrophy, while the underlying mechanisms for its protection against muscle atrophy are unknown. The present study was carried out to improve our understanding of the mechanism of DHEA’s protective effect on muscle cells. We observe...

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Veröffentlicht in:Applied biochemistry and biotechnology Jg. 176; H. 1; S. 22 - 32
Hauptverfasser: Jeon, Songhee, Hur, Jinyoung, Kim, Jongpil
Format: Journal Article
Sprache:Englisch
Veröffentlicht: New York Springer-Verlag 01.05.2015
Springer US
Springer Nature B.V
Schlagworte:
Animals
anti-inflammatory activity
antioxidant activity
Antioxidants
Biochemistry
Biotechnology
cell death
Cell Line
Cells
Chemistry
Chemistry and Materials Science
Dehydroepiandrosterone - pharmacology
dose response
Dystrophy
genes
Heme Oxygenase-1 - genetics
Heme Oxygenase-1 - metabolism
Hydrogen peroxide
Hydrogen Peroxide - pharmacology
MAP Kinase Signaling System - drug effects
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
mitogen-activated protein kinase
Muscle Proteins - genetics
Muscle Proteins - metabolism
muscles
muscular atrophy
Muscular Atrophy - drug therapy
Muscular Atrophy - genetics
Muscular Atrophy - metabolism
Muscular Atrophy - pathology
Muscular system
Myoblasts - metabolism
Myoblasts - pathology
myocytes
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
Oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - genetics
p38 Mitogen-Activated Protein Kinases - genetics
p38 Mitogen-Activated Protein Kinases - metabolism
phosphorylation
prasterone
protective effect
reactive oxygen species
Toxicity
Oxidative stress
HO-1
C
cells
p38
Nrf2
ISSN:0273-2289, 1559-0291, 1559-0291
Online-Zugang:Volltext
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Zusammenfassung:Dehydroepiandrosterone (DHEA) has been proposed to regulate muscle dystrophy, while the underlying mechanisms for its protection against muscle atrophy are unknown. The present study was carried out to improve our understanding of the mechanism of DHEA’s protective effect on muscle cells. We observed that DHEA significantly decreased the loss of cell death associated with H₂O₂-induced toxicity. Pretreating the muscle cells with DHEA led to a reduction of the intracellular accumulation of reactive oxygen species (ROS) in response to H₂O₂. In addition, DHEA reduced the H₂O₂-induced phosphorylation of ERK and p38 in a dose-dependent manner. Moreover, DHEA stimulated the activation of Nrf2, which led to the expression of an antioxidant response gene, HO-1. These results suggest that both antioxidants and anti-inflammatory properties mediate DHEA’s effects for protection against muscle atrophy.
Bibliographie:http://dx.doi.org/10.1007/s12010-015-1500-y
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ISSN:0273-2289
1559-0291
1559-0291
DOI:10.1007/s12010-015-1500-y