Abstract

Photo-aging is caused by cumulative oxidative stress from ultraviolet B irradiation with up-regulating intracellular reactive oxygen species, 4-hydroxynonenal, and matrix metalloproteinases. MMPs are the enzyme that degrades collagens so that impair the function of the dermis. Galangin was identified by 1H-NMR and 13C-NMR spectroscopy and is a natural flavonol that recently known to have many pharmacological effects such as anti-viral, anti-inflammatory, anti-atopic dermatitis and anti-oxidative activities. In this study, the protective effect of galangin on UVB-induced photo-aging in human skin fibroblasts (CCD-986sk) was conducted by Western blot analysis and enzyme-linked immunosorbent assay. Activator protein 1 and nuclear factor-kappa B are the main transcription factors from activated mitogen-activated protein kinases that up-regulates MMPs. Galangin showed down-regulation of intracellular ROS, 4-HNE, and MMPs through inhibition of phosphorylation of the MAPK pathway and showed a protective effect against skin fibroblasts under oxidative stress caused by UVB irradiation. This lead to up-regulation of fibroblast growth factor 2 and type 1 pro-collagen. These findings suggest that galangin can be developed as a potential agent for functional food and cosmetics of UVB-induced skin photo-aging.

Highlights

  • Skin aging can be caused by two types of aging factors: intrinsic aging factors and extrinsic aging factors

  • Ultraviolet-B (UVB) irradiation is known to be responsible for the biological damage on the skin more than UVA, and cause skin photo-aging by up-regulation of two transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kB), by producing reactive oxygen species (ROS) in human skin fibroblasts [4, 7]

  • The structure of galangin was identified by 1H-NMR and 13CNMR spectroscopy and this study were carried out to examine the effect of galangin on preventing photo-aging through mitogen-activated protein kinases (MAPKs) signaling pathways in UVB irradiated human skin fibroblasts

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Summary

Introduction

Skin aging can be caused by two types of aging factors: intrinsic aging factors and extrinsic aging factors. Ultraviolet-B (UVB) irradiation is known to be responsible for the biological damage on the skin more than UVA, and cause skin photo-aging by up-regulation of two transcription factors, activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kB), by producing ROS in human skin fibroblasts [4, 7]. These enzymes induce the generation of transcription factor AP-1, a heterodimer consisting of c-Jun and c-Fos. Phosphorylation of MAPKs results in activation of AP-1, causing gene expression of MMP-1, MMP-3, MMP-9 and inhibition of type 1 procollagen expression [8, 9].

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