Abietic acid inhibits UVB-induced MMP-1 expression in human dermal fibroblast cells through PPARα/γ dual activation.
- Abietic acid inhibits UVB-induced MMP-1 expression in human dermal fibroblast cells through PPARα/γ dual activation.
- 전영식; 정유정; 염종경; 강기성; 김용기; 김수남
- ap-1; MMPs; NF-kB; PPARa/r dual activator; abietic acid
- Issue Date
- Experimental dermatology
- VOL 24, NO 2, 140-145
- Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligandactivated transcription factors and consist of three isotypes: PPARa, PPARb/d and PPARc. PPARs are expressed in various cell types in the skin, including keratinocytes, fibroblasts and infiltrating immune cells. Thus, these receptors are highly studied
in dermato-endocrine research, and their ligands are targets for the treatment of various skin disorders, such as photoageing and chronological ageing of skin. Intensive studies have revealed that PPARa/c functions in photoageing and age-related inflammation by regulating matrix metalloproteinases (MMPs) via nuclear factor-kappa B (NF-jB) and activator protein-1 (AP-1). However, the detailed mechanism of PPARa/c’s role in photoageing has not yet been elucidated. In this study, we confirmed that abietic acid (AA) is a PPARa/c dual ligand and significantly decreased UVBinduced MMP-1 expression by downregulating UVB-induced MAPK signalling and downstream transcription factors, subsequently reducing IjBa degradation and blocking NF-jB p65 nuclear translocation in Hs68 human dermal fibroblast cells. Treatment of cells with AA and GW6471 or bisphenol A diglycidyl ether (BADGE), PPARa or PPARc antagonists, respectively, reversed the effect on UVB-induced MMP-1 expression and inflammatory signalling pathway activation. Taken together, our data suggest that AA acts as a PPARa/c dual activator to inhibit UVB-induced MMP-1 expression and agerelated inflammation by suppressing NF-jB and the MAPK/AP-1 pathway and can be a useful agent for improving skin photoageing.
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