ReferenceID 525

SS-31 attenuates TNF-α induced cytokine release from C2C12 myotubes

Redox Biol

TNF-α is a key inflammatory mediator and is proposed to induce transcriptional responses via the mitochondrial generation of Reactive Oxygen Species (ROS). The aim of this study was to determine the effect of TNF-α on t

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Reference Id
525
Evidence Id
17115
Core Evidence Id
17115
Source Reference Id
1018
Herb2 Reference Id
HBREF001740
Subject Paper Key
HBIN018821_26291279
Pubmed Id
26291279
Doi
10.1016/j.redox.2015.08.007
Paper Title
SS-31 attenuates TNF-α induced cytokine release from C2C12 myotubes
Paper Abstract
TNF-α is a key inflammatory mediator and is proposed to induce transcriptional responses via the mitochondrial generation of Reactive Oxygen Species (ROS). The aim of this study was to determine the effect of TNF-α on the production of myokines by skeletal muscle. Significant increases were seen in the release of IL-6, MCP-1/CCL2, RANTES/CCL5 and KC/CXCL1 and this release was inhibited by treatment with Brefeldin A, suggesting a golgi-mediated release of cytokines by muscle cells. An increase was also seen in superoxide in response to treatment with TNF-α, which was localised to the mitochondria and this was also associated with activation of NF-κB. The changes in superoxide, activation of NF-kB and release of myokines were attenuated following pre-treatment with SS-31 peptide indicating that the ability of TNF-α to induce myokine release may be mediated through mitochondrial superoxide, which is, at least in part, associated with activation of the redox sensitive transcription factor NF-kB.
Journal
Redox Biol
Publish Year
2015
Experiment Subject
muscle cells
Experiment Type
Cell Experiment
Phenotype Related
Paper Title Cn
Paper Title En
SS-31 attenuates TNF-α induced cytokine release from C2C12 myotubes
Bilingual Status
semi_complete