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Oleracone C from Portulaca oleracea attenuates UVB ‐induced changes in matrix metalloproteinase and type I procollagen production via MAPK and TGF ‐β/Smad pathways in human keratinocytes

光老化 前胶原肽酶 基质金属蛋白酶 化学 活性氧 分子生物学 p38丝裂原活化蛋白激酶 免疫印迹 活力测定 Ⅰ型胶原 SMAD公司 马齿苋 氧化应激 MAPK/ERK通路 细胞凋亡 生物化学 磷酸化 生物 内分泌学 植物 遗传学 基因
作者
Jung Hwan Oh,Fatih Karadeniz,Jung Im Lee,Youngwan Seo,Chang‐Suk Kong
出处
期刊:International Journal of Cosmetic Science [Wiley]
卷期号:45 (2): 166-176 被引量:9
标识
DOI:10.1111/ics.12828
摘要

BACKGROUND: Chronic exposure to ultraviolet (UV) radiation induces photo-oxidation, which in turn causes the overproduction of matrix metalloproteinases (MMPs) and collagen degradation. These symptoms are referred to as photoaging, which is characterized by skin thickness, irregular pigmentation, elastosis and coarse wrinkles. In this study, the protective effects of oleracone C isolated from Portulaca olerace against UVB-induced changes in MMPs and type I procollagen production were investigated in human keratinocytes. METHODS: Human immortalized keratinocytes have been used as an in vitro cell model to study the abnormal skin barrier development such as in photoaging. The effects of the compound on cell viability were determined by colorimetric MTT assay. This study also measured ROS production using DCFH-DA assay. Releases of MMPs and type Iα1 procollagen were analysed by ELISA. RT-PCR and Western blot were carried out to test the expressions of mRNA and proteins related to MMPs and type I procollagen biosynthesis. RESULT: Effect of oleracone C against UVB-mediated oxidative stress was evaluated measuring its ability to eliminate UVB-induced activation of reactive oxygen species (ROS). Treatment of oleracone C hindered the production of intracellular ROS. UVB exposure increased MMPs (MMP-1, MMP-2 and MMP-9) release from keratinocytes and decreased the release of type I procollagen. Treatment with oleracone C reversed these effects of UVB exposure. Oleracone C treatment also diminished the intracellular expression of MMP-1, MMP-2 and MMP-9 and elevated the type I procollagen. Oleracone C suppressed the UVB irradiation-dependent upregulation phosphorylation of p38 and ERK1/2 in the mitogen-activated protein kinase (MAPK) pathway. Furthermore, oleracone C stimulated collagen production through the TGF-β signalling pathway, which activates collagen synthesis in UVB-irradiated keratinocytes. CONCLUSION: These findings reasonably suggest ameliorating the potential of oleracone C against the UVB-induced photoaging of the human keratinocytes.
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