2'-Fucosyllactose Attenuates Particulate Matter-Induced Inflammation via Inhibition of Hypoxia-Inducible Factor in Keratinocytes
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- Lee Kyung-Eun
- COSMAX BTI R&I Center
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- Ryu Jung Jin
- COSMAX BTI R&I Center
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- Jo Young Kwan
- COSMAX R&I Center
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- Yeo Hyeonju
- COSMAX BTI R&I Center
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- Kang Seunghyun
- COSMAX BTI R&I Center
書誌事項
- タイトル別名
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- 2′-Fucosyllactose Attenuates Particulate Matter-Induced Inflammation <i>via</i> Inhibition of Hypoxia-Inducible Factor in Keratinocytes
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抄録
<p>2′-Fucosyllactose (2FL) is the most abundant component of the oligosaccharide content in human milk. It has been reported that 2FL has the ability to protect against infectious disease caused by bacterial pathogens. In this study, we investigated the protective effects of 2FL on particulate matter (PM)10-induced pro-inflammatory cytokines in HaCaT keratinocytes. 2FL reduced PM10-induced excess expression of interleukin (IL)-6, IL-8, IL-1α and IL-1β in HaCaT keratinocytes. In addition, PM10 also increased hypoxia-inducible factor (HIF)-1α protein levels; however, 2FL inhibited the accumulation of HIF-1α protein and the phosphorylation of phosphatidylinositol 3-kinase (PI3K)/Akt stimulated by PM10. Furthermore, 2FL improved PM10-induced the decrease in epidermal thickness and integrity of the cornified layer in the reconstructed human epidermal skin model (RHE). In our results, 2FL inhibited PM10-induced pro-inflammatory mediators by regulating the HIF-1α/PI3K/Akt pathway and protected the skin epidermis against PM10 irritation. Taken together, these results suggest that 2FL can be used as a primary ingredient in cosmeceutical products to alleviate skin irritation and inflammation caused by urban air pollution.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 42 (10), 1620-1627, 2019-10-01
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390564227317414272
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- NII論文ID
- 130007722433
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 029984214
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- PubMed
- 31582650
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可