Anticatabolic and Anti-Inflammatory Effects of Myricetin 3-O-β-d-Galactopyranoside in UVA-Irradiated Dermal Cells via Repression of MAPK/AP-1 and Activation of TGFβ/Smad.

Jung Hwan Oh,Jung Im Lee,Fatih Karadeniz,Youngwan Seo,So Young Park,Chang-Suk Kong

doi:10.3390/molecules25061331

Jung Hwan Oh, Jung Im Lee + Show 4 more

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https://doi.org/10.3390/molecules25061331

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Journal: Molecules	Publication Date: Mar 14, 2020
Citations: 30	License type: CC BY 4.0

Affiliation: Silla University, Korea Maritime and Ocean University

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UV irradiation is one of the main causes of extrinsic skin aging. UV-mediated skin aging, also known as photoaging, causes excessive breakdown of extracellular matrix which leads skin to lose its elasticity and strength. Several phytochemicals are known to exert anti-photoaging effects via different mechanisms, partly due to their antioxidant properties. The current study has been carried out to determine the potential anti-photoaging properties of myricetin 3-O-β-d-galacto-pyranoside (M3G), a flavonol glycoside isolated from L. tetragonum, in UVA-irradiated in vitro models; HaCaT keratinocytes and human dermal fibroblasts (HDFs). UVA-induced changes in MMP-1 and collagen production have been observed in HaCaT keratinocytes and HDFs. Further, UVA-induced activation of MAPK signaling, and pro-inflammatory cytokine production have been investigated. TGFβ/Smad pathway has also been analyzed in UVA-irradiated HDFs. Treatment with M3G reversed the UVA-induced changes in MMP-1 and collagen production both in HaCaT keratinocytes and HDFs. UVA-mediated activation of p38, ERK and JNK MAPK activation was also inhibited by M3G treatment in HaCaT keratinocytes. In HDFs, M3G was able to upregulate the TGFβ/Smad pathway activation. In addition, M3G downregulated the UVA-induced pro-inflammatory cytokines in keratinocytes and HDFs. It has been suggested that the M3G has exerted potential antiphotoaging properties in vitro, by attenuating UVA-induced changes in MMP-1 and collagen production in keratinocytes and dermal fibroblasts.

Highlights

Photoaging is the extrinsic aging of the human skin caused by ultraviolet radiation
It has been suggested that the myricetin 3-O-β-d-galactopyranoside (M3G) has exerted potential antiphotoaging properties in vitro, by attenuating UVA-induced changes in matrix metalloproteinases (MMPs)-1 and collagen production in keratinocytes and dermal fibroblasts
UVA exposure leads to detrimental changes in cellular pathways of the dermal fibroblasts where collagen and elastin degrading enzymes, matrix metalloproteinases (MMPs) and inflammatory response are stimulated via activator protein 1 (AP-1) mediated signaling [4,5]

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Introduction

Photoaging manifests itself with wrinkles and loss of elasticity due to increasing collagen and elastin damage and inflammatory response in the skin [1]. UVA exposure leads to detrimental changes in cellular pathways of the dermal fibroblasts where collagen and elastin degrading enzymes, matrix metalloproteinases (MMPs) and inflammatory response are stimulated via activator protein 1 (AP-1) mediated signaling [4,5]. As it penetrates deep parts of dermis, UVA exposure causes damages in dermal fibroblasts, where the collagen is produced to give skin its firmness [6]. Increasing production of MMPs and diminished collagen formation are among main reasons behind UVA mediated damage in dermal layer

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