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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Vydané v:	Applied biochemistry and biotechnology Ročník 176; číslo 1; s. 22 - 32
Hlavní autori:	Jeon, Songhee, Hur, Jinyoung, Kim, Jongpil
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	New York Springer-Verlag 01.05.2015 Springer US Springer Nature B.V
Predmet:	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
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Abstract	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.
AbstractList	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. 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.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. 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. 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 H 2 O 2 -induced toxicity. Pretreating the muscle cells with DHEA led to a reduction of the intracellular accumulation of reactive oxygen species (ROS) in response to H 2 O 2 . In addition, DHEA reduced the H 2 O 2 -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.
Author	Jeon, Songhee Hur, Jinyoung Kim, Jongpil
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publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2010.05.011
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SubjectTerms	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
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Title	DHEA Alleviates Oxidative Stress of Muscle Cells via Activation of Nrf2 Pathway
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