S-Space Graduate School of Convergence Science and Technology (융합과학기술대학원) Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과) Journal Papers (저널논문_분자의학 및 바이오제약학과)
Piceatannol inhibits phorbol ester-induced expression of COX-2 and iNOS in HR-1 hairless mouse skin by blocking the activation of NF-kappa B and AP-1
- Liu, Lijia; Li, Jianchun; Kundu, Joydeb Kumar; Surh, Young-Joon
- Issue Date
- Inflammation Research, Vol.63 No.12, pp.1013-1021
- Piceatannol; Cyclooxygenase-2; Inducible nitric oxide synthase; Nuclear factor-kappaB; Activator protein-1; Mouse skin
- The present study was aimed at elucidating the molecular mechanisms of anti-inflammatory activity of piceatannol (trans-3,4,3',5'-tetrahydroxystilbene) in mouse skin in vivo. Female HR-1 hairless mice were topically treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) with or without piceatannol pretreatment. Epidermal protein expression was assessed by Western blot analysis. The cyclooxygenase-2 (COX-2) expression was detected by immunohistochemistry. The DNA binding of nuclear factor-kappaB (NF-kappa B) and activator protein-1 (AP-1) was examined by the electrophoretic mobility gel shift assay. The catalytic activity of I kappa B alpha kinase-beta (IKK beta) was measured by in vitro kinase assay. Pretreatment with piceatannol attenuated TPA-induced expression of COX-2 and inducible nitric oxide synthase (iNOS) in mouse skin. Piceatannol diminished nuclear translocation and the DNA binding of NF-kappa B through the blockade of phosphorylation and subsequent degradation of I kappa B alpha. Piceatannol attenuated the catalytic activity of IKK beta and inhibited the phosphorylation of mitogen-activated protein (MAP) kinases in TPA-treated mouse skin. In addition, piceatannol decreased TPA-induced expression of c-Fos and the DNA binding of AP-1. Piceatannol inhibits TPA-induced COX-2 and iNOS expression by blocking the activation of NF-kappa B and AP-1 via suppression of the IKK beta activity and phosphorylation of MAP kinases, which provides a mechanistic basis of its anti-inflammatory effects in mouse skin.
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