Skeletal Muscle Nrf2 Contributes to Exercise-Evoked Systemic Antioxidant Defense Via Extracellular Vesicular Communication: Corrigendum

2021 ◽  
Vol 49 (4) ◽  
pp. 294-294
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Defense

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Mapk Signaling ◽  
Redox Signaling ◽  
Defense System ◽  
High Fat ◽  
Substrate Metabolism ◽  
Endogenous Antioxidant

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.

Cinnamaldehyde regulates H2O2-induced skeletal muscle atrophy by ameliorating the proteolytic and antioxidant defense systems

2018 ◽  
Vol 234 (5) ◽  
pp. 6194-6208 ◽  
Author(s):  
Nirmaljeet Kaur ◽  
Prachi Gupta ◽  
Vikram Saini ◽  
Sandeep Sherawat ◽  
Sanjeev Gupta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Antioxidant Defense ◽  
Skeletal Muscle Atrophy ◽  
Defense Systems ◽  
Antioxidant Defense Systems

scholarly journals A Combination of Lipoic Acid Plus Coenzyme Q10 Induces PGC1α, a Master Switch of Energy Metabolism, Improves Stress Response, and Increases Cellular Glutathione Levels in Cultured C2C12 Skeletal Muscle Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
A. E. Wagner ◽  
I. M. A. Ernst ◽  
M. Birringer ◽  
Ö. Sancak ◽  
L. Barella ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stress Response ◽  
Energy Metabolism ◽  
Lipoic Acid ◽  
Coenzyme Q10 ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Combined Supplementation

Skeletal muscle function largely depend on intact energy metabolism, stress response, and antioxidant defense mechanisms. In this study, we tested the effect of a combined supplementation ofα-lipoic acid (LA) plus coenzyme Q10 (Q10) on PPARγ-coactivatorα(PGC1α) activity, expression of glutathione-related phase II enzymes and glutathione (GSH) levels in cultured C2C12 myotubes. Supplementation of myotubes with 250 μmol/L LA plus 100 μmol/L Q10 significantly increased nuclear levels of PGC1α, a master switch of energy metabolism and mitochondrial biogenesis. The increase of nuclear PGC1αwas accompanied by an increase in PPARγtransactivation, a downstream target of PGC1α, and an increase in mitochondrial transcription factor A mRNA centrally involved in mitochondrial replication and transcription. Furthermore, supplementation of myotubes with LA plus Q10 resulted in an increase of genes encoding proteins involved in stress response, GSH synthesis, and its recycling. In LA-plus-Q10-treated myotubes a significant 4-fold increase in GSH was evident. This increase in GSH was accompanied by increased nuclear Nrf2 protein levels, partly regulatingγGCS and GST gene expression. Present data suggest that the combined supplementation of skeletal muscle cells with LA plus Q10 may improve energy homeostasis, stress response, and antioxidant defense mechanisms.

scholarly journals BQ123 Stimulates Skeletal Muscle Antioxidant Defense via Nrf2 Activation in LPS-Treated Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Agata Kowalczyk ◽  
Agnieszka Jeleń ◽  
Marta Żebrowska ◽  
Ewa Balcerczak ◽  
Anna Gorąca
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Saline Control ◽  
B Subunit ◽  
Lps Challenge ◽  
Endothelin A Receptor ◽  
Femoral Muscle ◽  
Male Wistar Rats ◽  
Endothelin A

Little is understood of skeletal muscle tissue in terms of oxidative stress and inflammation. Endothelin-1 is an endogenous, vasoconstrictive peptide which can induce overproduction of reactive oxygen species and proinflammatory cytokines. The aim of this study was to evaluate whether BQ123, an endothelin-A receptor antagonist, influences the level of TNF-α, IL-6, SOD-1, HO-1, Nrf2 mRNA, and NF-κB subunit RelA/p65 mRNA in the femoral muscle obtained from endotoxemic rats. Male Wistar rats were divided into 4 groups (n=6) and receivediv(1) saline (control), (2) LPS (15 mg/kg), (3) BQ123 (1 mg/kg), (4) BQ123 (1 mg/kg), and LPS (15 mg/kg, resp.) 30 min later. Injection of LPS led to significant increase in levels of RelA/p65 mRNA, TNF-α, and IL-6, while content of SOD-1, HO-1, and Nrf2 mRNA was unchanged. Administration of BQ123 prior to LPS challenge resulted in a significant reduction in RelA/p65 mRNA, TNF-α, and IL-6 levels, as well as markedly elevated concentrations of SOD-1, HO-1, and Nrf2 mRNA. BQ123 appears to enhance antioxidant defense and prevent production of TNF-αand IL-6 in skeletal muscle of LPS-treated rat. In conclusion, endothelin-A receptor antagonism exerts significant impact on the skeletal muscle favouring anti-inflammatory effects and protection against oxidative stress.

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