<i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1
Atopic dermatitis (AD) is a skin allergy accompanied by acute and chronic dermal inflammation. In traditional oriental medicine, <i>Laminaria japonica</i> has been used to treat various diseases, including inflammatory diseases. Therefore, to determine the therapeutic potential of <i&...
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2020-10-01
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author | Youn-Hwan Hwang Hyun-Kyung Song Ami Lee Hyunil Ha Taesoo Kim |
author_facet | Youn-Hwan Hwang Hyun-Kyung Song Ami Lee Hyunil Ha Taesoo Kim |
author_sort | Youn-Hwan Hwang |
collection | DOAJ |
description | Atopic dermatitis (AD) is a skin allergy accompanied by acute and chronic dermal inflammation. In traditional oriental medicine, <i>Laminaria japonica</i> has been used to treat various diseases, including inflammatory diseases. Therefore, to determine the therapeutic potential of <i>L. japonica</i> against AD, we investigated the inhibitory effects of <i>L. japonica</i> water extract (LJWE) on the inflammatory mediators and AD-like skin lesions. We determined the cell viability of LJWE-treated HaCaT cells using the cell counting kit-8 assay and the levels of inflammatory cytokines using cytometric bead array kits. Additionally, we analyzed the modulatory effects of LJWE on the signaling pathways in tumor necrosis factor-α/interferon-γ-stimulated HaCaT cells via Western blotting. Furthermore, we determined the in vivo effect of LJWE on NC/Nga mice and found that LJWE remarkably improved the skin moisture, reduced dermatitis severity, and inhibited the overproduction of inflammatory mediators in 2,4-dinitrochlorobenzene-sensitized NC/Nga mice. We also observed that LJWE inhibits the expression of inflammatory chemokines in human keratinocytes by downregulating the p38 mitogen-activated protein kinase signaling pathway and activating the signal transducer and activator of transcription 1. In conclusion, LJWE has the therapeutic potential against AD by healing AD-like skin lesions, and suppressing inflammatory mediators and major signaling molecules. |
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spelling | doaj.art-3d08dfebc5e44757a302d7cf1fe11c732023-11-20T18:12:52ZengMDPI AGNutrients2072-66432020-10-011211323810.3390/nu12113238<i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1Youn-Hwan Hwang0Hyun-Kyung Song1Ami Lee2Hyunil Ha3Taesoo Kim4Herbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, KoreaHerbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, KoreaHerbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, KoreaHerbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, KoreaHerbal Medicine Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, KoreaAtopic dermatitis (AD) is a skin allergy accompanied by acute and chronic dermal inflammation. In traditional oriental medicine, <i>Laminaria japonica</i> has been used to treat various diseases, including inflammatory diseases. Therefore, to determine the therapeutic potential of <i>L. japonica</i> against AD, we investigated the inhibitory effects of <i>L. japonica</i> water extract (LJWE) on the inflammatory mediators and AD-like skin lesions. We determined the cell viability of LJWE-treated HaCaT cells using the cell counting kit-8 assay and the levels of inflammatory cytokines using cytometric bead array kits. Additionally, we analyzed the modulatory effects of LJWE on the signaling pathways in tumor necrosis factor-α/interferon-γ-stimulated HaCaT cells via Western blotting. Furthermore, we determined the in vivo effect of LJWE on NC/Nga mice and found that LJWE remarkably improved the skin moisture, reduced dermatitis severity, and inhibited the overproduction of inflammatory mediators in 2,4-dinitrochlorobenzene-sensitized NC/Nga mice. We also observed that LJWE inhibits the expression of inflammatory chemokines in human keratinocytes by downregulating the p38 mitogen-activated protein kinase signaling pathway and activating the signal transducer and activator of transcription 1. In conclusion, LJWE has the therapeutic potential against AD by healing AD-like skin lesions, and suppressing inflammatory mediators and major signaling molecules.https://www.mdpi.com/2072-6643/12/11/3238<i>Laminaria japonica</i>atopic dermatitisHaCaT cellsNC/Nga mice |
spellingShingle | Youn-Hwan Hwang Hyun-Kyung Song Ami Lee Hyunil Ha Taesoo Kim <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 Nutrients <i>Laminaria japonica</i> atopic dermatitis HaCaT cells NC/Nga mice |
title | <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 |
title_full | <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 |
title_fullStr | <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 |
title_full_unstemmed | <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 |
title_short | <i>Laminaria japonica</i> Suppresses the Atopic Dermatitis-Like Responses in NC/Nga Mice and Inflamed HaCaT Keratinocytes via the Downregulation of STAT1 |
title_sort | i laminaria japonica i suppresses the atopic dermatitis like responses in nc nga mice and inflamed hacat keratinocytes via the downregulation of stat1 |
topic | <i>Laminaria japonica</i> atopic dermatitis HaCaT cells NC/Nga mice |
url | https://www.mdpi.com/2072-6643/12/11/3238 |
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