The role of NADPH oxidase 2 in regulating IL-15 and PGC-1α gene expressions following a period of high intensity interval training: [The original title and the article is written in Persian!]

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Introduction: Following trainging, Reactive Oxygen Spices (ROS) play a crucial role in the regulation of signaling pathways and adaptions in skeletal muscle, including mitochondrial biogenesis and improvement in insulin sensitivity a ROS-induced physical activity can also stimulate myokine production in skeletal muscle. The aim of this work was hence to investigate the role of NADPH Oxidase-2 (NOX2), the main source of ROS generation, in contracting muscle in IL-15 gene expression, as well as anychanges in PGC-1α, as a key regulator of mitochondrial biogenesis, following a period of High-intensity Interval Training (HIIT).

Materials and Methods: Mice were divided into four groups: Wild type (WT) control (WTc) and training (WTt), NOX-2 deficient (ND) control (NDc) and training (NDt). Training groups performed 6-week HIIT, including 2-min running intervals with 100% of their maximum running speed and 2-min rest with 30% of this speed for a total of 60 min; speed was increased 1m/min each week. IL-15, PGC-1α and NOX2 mRNA levels in gastrocnemius muscle were analyzed using Real time.

Results: Basal levels of IL-15 mRNA in NDc group were significantly lower than the other groups. Relative gene expression in WTc, WTt, NDc and NDt changed for IL-15 1, 1.15, 0.49 and 0.99 and for PGC-1α 1, 1.73. 0.76 and 1.4 times, respectively in WTt. Post-training muscle PGC-1α mRNA levels increased significantly.

Conclusion: Results indicate that IL-15 gene expression in mouse skeletal muscle is dependent on NOX2. And apparently NOX2 deficiency may result in impaired PGC-1α expression and subsequently diminished mitochondrial biogenesis.

OriginalsprogUdefineret/Ukendt
TidsskriftIranian Journal of Endocrinology and Metabolism
Vol/bind20
Udgave nummer5
Sider (fra-til)263-272
Antal sider10
ISSN1683-4844
StatusUdgivet - 2019

Bibliografisk note

CURIS 2019 NEXS 112

ID: 215782253