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Codonopsis laceolata Water Extract Ameliorates Asthma Severity by Inducing Th2 Cells' and Pulmonary Epithelial Cells' Apoptosis via NF-κB/COX-2 Pathway

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dc.contributor.authorBok, So-Hyeon-
dc.contributor.authorHan, Kang Min-
dc.contributor.authorBoo, Hee-Ock-
dc.contributor.authorCho, Seung-Sik-
dc.contributor.authorPark, Dae-Hun-
dc.date.accessioned2023-04-27T10:40:50Z-
dc.date.available2023-04-27T10:40:50Z-
dc.date.issued2022-07-
dc.identifier.issn2227-9717-
dc.identifier.issn2227-9717-
dc.identifier.urihttps://scholarworks.dongguk.edu/handle/sw.dongguk/2895-
dc.description.abstractAsthma is an incurable pulmonary disease with several symptoms, including abnormal breathing, coughing, and sleep apnea, which can lead to death, and the population of asthma patients has been increasing worldwide. There are many adverse effects in current drugs, and thus, we have tried to develop anti-asthmatic agents from natural products such as Codonopsis laceolata. To define the anti-asthmatic effect and the mechanism of Codonopsis laceolata, an animal study was conducted considering different cell counts of BALF, serum IgE levels, morphological changes in the pulmonary system, the Th2 cell transcription factor (GATA-3), and the apoptotic pathway (NF-kappa B/COX-2). Codonopsis laceolata significantly suppressed the representative asthmatic changes, such as airway remodeling, mucous hypersecretion, epithelial hyperplasia, and inflammatory cell infiltration, in the respiratory system. It suppressed the levels of GATA-3, IL-4, and IL-13. The down-regulation of Th2-related factors, such as GATA-3, IL-4, and IL-13, results from the stimulated apoptosis of Th2 cells and epithelial cells via a decrease in the levels of NF-kappa B and COX-2. We concluded that Codonopsis laceolata might be a promising anti-asthmatic drug.-
dc.format.extent13-
dc.language영어-
dc.language.isoENG-
dc.publisherMDPI-
dc.titleCodonopsis laceolata Water Extract Ameliorates Asthma Severity by Inducing Th2 Cells' and Pulmonary Epithelial Cells' Apoptosis via NF-κB/COX-2 Pathway-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.3390/pr10071249-
dc.identifier.scopusid2-s2.0-85133206448-
dc.identifier.wosid000832410500001-
dc.identifier.bibliographicCitationProcesses, v.10, no.7, pp 1 - 13-
dc.citation.titleProcesses-
dc.citation.volume10-
dc.citation.number7-
dc.citation.startPage1-
dc.citation.endPage13-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEngineering-
dc.relation.journalWebOfScienceCategoryEngineering, Chemical-
dc.subject.keywordPlusIFN-GAMMA-
dc.subject.keywordPlusT-BET-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusLANCEOLATA-
dc.subject.keywordPlusINTERLEUKIN-12-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusCYTOKINES-
dc.subject.keywordAuthorCodonopsis laceolata-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorNF-kappa B/COX-2 pathway-
dc.subject.keywordAuthorasthma severity-
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