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    Resveratrol modulates interleukin-1beta-induced phosphatidylinositol 3-kinase and nuclear factor kappaB signaling pathways in human tenocytes

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    Publication date
    2012
    Author
    Busch, F.
    Mobasheri, A.
    Shayan, P.
    Lueders, C.
    Stahlmann, R.
    Shakibaei, M.
    Keyword
    Androstadienes; Pharmacology;
    Anti-inflammatory agents; Non-Steroidal;
    Apoptosis; Drug effects;
    Blotting; Western;
    Cells, Cultured
    Collagen; Metabolism;
    Dose-response relationship;
    Humans;
    Inositol phosphates;
    Interleukin-1beta;
    Male;
    Microscopy; Electron;
    Middle aged;
    Mitochondria;
    NF-kappa B/*metabolism;
    Phosphatidylinositol 3-Kinase; Antagonists & inhibitors;
    Phosphorylation;
    Proto-oncogene proteins c-akt;
    Pyrazoles;
    Pyrimidines;
    Signal transduction;
    Sirtuin 1;
    Stilbenes;
    Tendons/cytology;
    Time factors;
    src-Family Kinases;
    REF 2014
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    Abstract
    Resveratrol, an activator of histone deacetylase Sirt-1, has been proposed to have beneficial health effects due to its antioxidant and anti-inflammatory properties. However, the mechanisms underlying the anti-inflammatory effects of resveratrol and the intracellular signaling pathways involved are poorly understood. An in vitro model of human tenocytes was used to examine the mechanism of resveratrol action on IL-1beta-mediated inflammatory signaling. Resveratrol suppressed IL-1beta-induced activation of NF-kappaB and PI3K in a dose- and time-dependent manner. Treatment with resveratrol enhanced the production of matrix components collagen types I and III, tenomodulin, and tenogenic transcription factor scleraxis, whereas it inhibited gene products involved in inflammation and apoptosis. IL-1beta-induced NF-kappaB and PI3K activation was inhibited by resveratrol or the inhibitors of PI3K (wortmannin), c-Src (PP1), and Akt (SH-5) through inhibition of IkappaB kinase, IkappaBalpha phosphorylation, and inhibition of nuclear translocation of NF-kappaB, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-kappaB activation. Inhibition of PI3K by wortmannin attenuated IL-1beta-induced Akt and p65 acetylation, suggesting that p65 is a downstream component of PI3K/Akt in these responses. The modulatory effects of resveratrol on IL-1beta-induced activation of NF-kappaB and PI3K were found to be mediated at least in part by the association between Sirt-1 and scleraxis and deacetylation of NF-kappaB and PI3K. Overall, these results demonstrate that activated Sirt-1 plays an essential role in the anti-inflammatory effects of resveratrol and this may be mediated at least in part through inhibition/deacetylation of PI3K and NF-kappaB.
    URI
    http://hdl.handle.net/10454/5903
    Citation
    Busch, F., Mobasheri, A., Shayan, P., Lueders, C., Stahlmann, R., Shakibaei, M. (2012) Resveratrol modulates interleukin-1beta-induced phosphatidylinositol 3-kinase and nuclear factor kappaB signaling pathways in human tenocytes. The Journal of Biological Chemistry, 287 (45), 38050-38063.
    Link to publisher’s version
    http://dx.doi.org/10.1074/jbc.M112.377028
    Type
    Article
    Collections
    Life Sciences Publications

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