Anti-inflammatory effects of Lagerstroemia ovalifolia Teijsm. & Binn. in TNFα/IFNγ-stimulated keratinocytes = 라저스트로에미아 오발리폴리아의 항염 효과

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dc.contributor.authorHan-Sol Lee-
dc.contributor.authorJin Hyub Paik-
dc.contributor.authorOk-Kyoung Kwon-
dc.contributor.authorI Paryanto-
dc.contributor.authorP Yuniato-
dc.contributor.authorHyung Won Ryu-
dc.contributor.authorSang-Ho Choi-
dc.contributor.authorSei-Ryang Oh-
dc.contributor.authorS B Han-
dc.contributor.authorJi Won Park-
dc.contributor.authorKyung Seop Ahn-
dc.date.accessioned2021-11-16T15:30:21Z-
dc.date.available2021-11-16T15:30:21Z-
dc.date.issued2021-
dc.identifier.issn1741-427X-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/25006-
dc.description.abstractEthnopharmacological Relevance. Atopic dermatitis is a chronic inflammatory skin disease. Lagerstroemia ovalifolia Teijsm. & Binn. (LO) has traditionally been used as an herbal medicine for anti-inflammatory diseases. The effect of LO on atopic dermatitis has not been verified scientifically. We investigated the effects of CHCl3 fraction number 5 of LO (LOC) on atopic dermatitis through cell-based experiments. HaCaT cells were treated with tumor necrosis factor-alpha (TNFα)/interferon-gamma (IFNγ) to induce an inflammatory reaction. Proinflammatory cytokines, interleukin- (IL-) 6, IL-8, and IL-1β and chemokines such as thymus and activation-regulated chemokine (TARC/CCL17), monocyte chemoattractant protein 1 (MCP1/CCL2), and macrophage-derived chemokine (MDC/CCL22) were measured by RT-PCR and ELISA. In addition, the degree of phosphorylation and activation of JAK/STAT1, PI3K/AKT, and nuclear factor-kappa B (NF-κB) were measured by western blot and luciferase assays. The production of inflammatory cytokines and chemokines and activation of the JAK/STAT1, PI3K/AKT, and NF-κB pathways were induced by TNFα/IFNγ in HaCaT cells. Under these conditions, LOC treatment inhibited the production of targeted cytokines and chemokines and decreased the phosphorylation and activation of JAK/STAT1, PI3K/AKT, and NF-κB. These results suggest that LOC reduces the production of proinflammatory cytokines and chemokines by suppressing the JAK/STAT1, PI3K/AKT, and NF-κB pathways. Therefore, LOC may have potential as a drug for atopic dermatitis.-
dc.publisherHindawi Ltd-
dc.titleAnti-inflammatory effects of Lagerstroemia ovalifolia Teijsm. & Binn. in TNFα/IFNγ-stimulated keratinocytes = 라저스트로에미아 오발리폴리아의 항염 효과-
dc.title.alternativeAnti-inflammatory effects of Lagerstroemia ovalifolia Teijsm. & Binn. in TNFα/IFNγ-stimulated keratinocytes-
dc.typeArticle-
dc.citation.titleEvidence-Based Complementary and Alternative Medicine-
dc.citation.number0-
dc.citation.endPage2439231-
dc.citation.startPage2439231-
dc.citation.volume2021-
dc.contributor.affiliatedAuthorHan-Sol Lee-
dc.contributor.affiliatedAuthorJin Hyub Paik-
dc.contributor.affiliatedAuthorOk-Kyoung Kwon-
dc.contributor.affiliatedAuthorHyung Won Ryu-
dc.contributor.affiliatedAuthorSang-Ho Choi-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.affiliatedAuthorJi Won Park-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.alternativeName이한솔-
dc.contributor.alternativeName백진협-
dc.contributor.alternativeName권옥경-
dc.contributor.alternativeNameParyanto-
dc.contributor.alternativeNameYuniato-
dc.contributor.alternativeName류형원-
dc.contributor.alternativeName최상호-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName한상배-
dc.contributor.alternativeName박지원-
dc.contributor.alternativeName안경섭-
dc.identifier.bibliographicCitationEvidence-Based Complementary and Alternative Medicine, vol. 2021, pp. 2439231-2439231-
dc.identifier.doi10.1155/2021/2439231-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > International Biological Material Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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