Details

Autor(en) / Beteiligte

• Jeon, Youngsic
• Jung, Yujung
• Kim, Min Cheol
• Kwon, Hak Cheol
• Kang, Ki Sung
• Kim, Yong Kee
• Kim, Su-Nam

Titel

Sargahydroquinoic acid inhibits TNFα-induced AP-1 and NF-κB signaling in HaCaT cells through PPARα activation

Ist Teil von

• Biochemical and biophysical research communications, 2014-08, Vol.450 (4), p.1553-1559

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2014

Quelle

MEDLINE

Beschreibungen/Notizen

• [Display omitted] •SHQA increases PPARα/γ transactivation and inhibits MMP-2/-9 expression.•SHQA inhibits TNFα-induced AP-1 and MAPK signaling.•SHQA inhibits TNFα-induced p65 translocation and IκBα phosphorylation.•SHQA inhibits TNFα-induced AP-1 and NF-κB signaling via PPARα. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors and expressed in various cell types in the skin, including keratinocytes, fibroblasts and infiltrating immune cells. Thus, their ligands are targets for the treatment of various skin disorders, such as photo-aging and chronological aging of skin. Intensive studies have revealed that PPARα/γ functions in photo-aging and age-related inflammation by regulating matrix metalloproteinases (MMPs) via activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). However, the detailed mechanism of PPARα/γ’s role in skin aging has not yet been elucidated. In this study, we confirmed that sargahydroquinoic acid (SHQA) as a PPARα/γ ligand significantly decreased Tumor Necrosis Factor-alpha (TNFα)-induced MMP-2/-9 expression by downregulating TNFα-induced transcription factors, subsequently reducing IκBα degradation and blocking NF-κB p65 nuclear translocation in HaCaT human epidermal keratinocyte cells. Treatment of cells with SHQA and GW6471 (PPARα antagonist) not bisphenol A diglycidyl ether (PPARγ antagonists), reversed the effect on TNFα-induced inflammatory signaling pathway activation. Taken together, our data suggest that SHQA inhibit TNFα-induced MMP-2/-9 expression and age-related inflammation by suppressing AP-1 and NF-κB pathway via PPARα.