3-Bromo-4,5-dihydroxybenzaldehyde isolated from Polysiphonia morrowii suppresses TNF-α/IFN-γ-stimulated inflammation and deterioration of skin barrier in HaCaT keratinocytes

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dc.contributor.authorA M K Jayasinghe-
dc.contributor.authorE J Han-
dc.contributor.authorK G I S Kirindage-
dc.contributor.authorI P S Fernando-
dc.contributor.authorE A Kim-
dc.contributor.authorJ Kim-
dc.contributor.authorKyungsook Jung-
dc.contributor.authorK N Kim-
dc.contributor.authorS J Heo-
dc.contributor.authorG Ahn-
dc.date.accessioned2022-09-26T16:33:00Z-
dc.date.available2022-09-26T16:33:00Z-
dc.date.issued2022-
dc.identifier.issn1660-3397-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/30386-
dc.description.abstractPolysiphonia morrowii is a well-known red alga that has promising pharmacological characteristics. The current study evaluates the protective effect of 3-bromo-4,5-dihydroxybenzaldehyde (BDB) isolated from P. morrowii on tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated inflammation and skin barrier deterioration in HaCaT keratinocytes. The anti-inflammatory effect of BDB in TNF-α/IFN-γ-stimulated HaCaT keratinocytes is evaluated by investigating nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, inflammatory cytokines, and chemokines. Further, the interaction between BDB and the skin barrier functions in stimulated HaCaT keratinocytes is investigated. The findings of the study reveal that BDB dose-dependently increases cell viability while decreasing intracellular reactive oxygen species (ROS) production. BDB downregulates the expression of inflammatory cytokines, interleukin (IL)-6, -8, -13, IFN-γ, TNF-α, and chemokines, Eotaxin, macrophage-derived chemokine (MDC), regulated on activation, normal T cells expressed and secreted (RANTES), and thymus and activation-regulated chemokine (TARC) by modulating the MAPK and NF-κB signaling pathways in TNF-α/IFN-γ-stimulated HaCaT keratinocytes. Furthermore, BDB increases the production of skin hydration proteins and tight junction proteins in stimulated HaCaT keratinocytes by preserving skin moisturization and tight junction stability. These findings imply that BDB exhibits a protective ability against inflammation and deterioration of skin barrier via suppressing the expression of inflammatory signaling in TNF-α/IFN-γ-stimulated HaCaT keratinocytes.-
dc.publisherMDPI-
dc.title3-Bromo-4,5-dihydroxybenzaldehyde isolated from Polysiphonia morrowii suppresses TNF-α/IFN-γ-stimulated inflammation and deterioration of skin barrier in HaCaT keratinocytes-
dc.title.alternative3-Bromo-4,5-dihydroxybenzaldehyde isolated from Polysiphonia morrowii suppresses TNF-α/IFN-γ-stimulated inflammation and deterioration of skin barrier in HaCaT keratinocytes-
dc.typeArticle-
dc.citation.titleMarine Drugs-
dc.citation.number9-
dc.citation.endPage563-
dc.citation.startPage563-
dc.citation.volume20-
dc.contributor.affiliatedAuthorKyungsook Jung-
dc.contributor.alternativeNameJayasinghe-
dc.contributor.alternativeName한의정-
dc.contributor.alternativeNameKirindage-
dc.contributor.alternativeNameFernando-
dc.contributor.alternativeName김은아-
dc.contributor.alternativeName김준성-
dc.contributor.alternativeName정경숙-
dc.contributor.alternativeName김길남-
dc.contributor.alternativeName허수진-
dc.contributor.alternativeName안긴내-
dc.identifier.bibliographicCitationMarine Drugs, vol. 20, no. 9, pp. 563-563-
dc.identifier.doi10.3390/md20090563-
dc.subject.keywordPolysiphonia morrowii-
dc.subject.keyword3-bromo-4,5-dihydroxybenzaldehyde-
dc.subject.keywordHaCaT keratinocyte-
dc.subject.keywordAntiinflammation-
dc.subject.keywordSkin barrier-
dc.subject.localPolysiphonia morrowii-
dc.subject.local3-bromo-4,5-dihydroxybenzaldehyde-
dc.subject.localHaCaT keratinocyte-
dc.subject.localAnti-inflammation-
dc.subject.localAntiinflammation-
dc.subject.localanti-inflammation-
dc.subject.localAnti-Inflammation-
dc.subject.localantiinflammation-
dc.subject.localSkin barrier-
dc.subject.localSkin Barrier-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
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