Protective effect of myokine IL-15 against H2O 2-mediated oxidative stress in skeletal muscle cells

The production of reactive oxygen species (ROS) during oxidative stress may cause cellular injury. Interleukin-15 (IL-15) is one of the skeletal muscle secreted myokines, and there is no information that reported its anti-oxidative capability in skeletal muscle. The aim of this study therefore is to...

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Bibliographic Details
Published in:Molecular biology reports 2014, Vol.41 (11), p.7715-7722
Main Authors: Li, Fengna, Li, Yinghui, Tang, Yulong, Lin, Binbin, Kong, Xiangfeng, Oladele, Oso Abimbola, Yin, Yulong
Format: Article
Language:English
Subjects:
cell viability
creatine kinase
gene expression
hydrogen peroxide
interleukin-6
lactate dehydrogenase
messenger RNA
myoblasts
myocytes
oxidative stress
protective effect
signal transduction
skeletal muscle
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Summary:The production of reactive oxygen species (ROS) during oxidative stress may cause cellular injury. Interleukin-15 (IL-15) is one of the skeletal muscle secreted myokines, and there is no information that reported its anti-oxidative capability in skeletal muscle. The aim of this study therefore is to investigate the protective effects of myokine IL-15 against H₂O₂-mediated oxidative stress in C2C12 myoblasts. The results showed that IL-15 pre-incubation reduced the intracellular creatine kinase and lactate dehydrogenase activities, decreased the ROS overload, and protect the mitochondrial network via up-regulated mRNA expression levels of IL-15 and uncoupling protein 3. It also down-regulated the levels of IL-6 and p21 of the myoblasts compared to the cells treated only with H₂O₂. Meanwhile, apurinic/aprimidinic endonuclease 1 expression and the Akt signaling pathway were stimulated. These effects could contribute to the resumption of cell viability and act as protective mechanism. In conclusion, myokine IL-15 could be a novel endogenous regulator to control intracellular ROS production and attenuate oxidative stress in skeletal muscle cells.
ISSN:0301-4851
1573-4978