Picrasma quassiodes (D. Don) Benn. attenuates lipopolysaccharide (LPS)-induced acute lung injury = 소태나무의 LPS-유도 급성폐손상 완화 효과

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dc.contributor.authorJae Won Lee-
dc.contributor.authorJi Won Park-
dc.contributor.authorNa Rae Shin-
dc.contributor.authorSo Yeon Park-
dc.contributor.authorOk-Kyoung Kwon-
dc.contributor.authorHyun Ah Park-
dc.contributor.authorYourim Lim-
dc.contributor.authorHyung Won Ryu-
dc.contributor.authorHeung Joo Yuk-
dc.contributor.authorJung Hee Kim-
dc.contributor.authorSei-Ryang Oh-
dc.contributor.authorKyung Seop Ahn-
dc.date.accessioned2017-04-19T10:25:17Z-
dc.date.available2017-04-19T10:25:17Z-
dc.date.issued2016-
dc.identifier.issn1107-3756-
dc.identifier.uri10.3892/ijmm.2016.2669ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13370-
dc.description.abstractPicrasma quassiodes (D.Don) Benn. (PQ) is a medicinal herb belonging to the family Simaroubaceae and is used as a traditional herbal remedy for various diseases. In this study, we evaluated the effects of PQ on airway inflammation using a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and LPS-stimulated RAW 264.7 cells. ALI was induced in C57BL/6 mice by the intranasal administration of LPS, and PQ was administered orally 3 days prior to exposure to LPS. Treatment with PQ significantly attenuated the infiltration of inflammatory cells in the bronchoalveolar lavage fluid (BALF). PQ also decreased the production of reactive oxygen species (ROS) and pro-inflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin (IL)-6 in BALF. In addition, PQ inhibited airway inflammation by reducing the expression of inducible nitric oxide synthase (iNOS) and by increasing the expression of heme oxygenase-1 (HO-1) in the lungs. Furthermore, we demonstrated that PQ blocked the activation of mitogen-activated protein kinase (MAPK) and nuclear factorB (NFB) in the lungs of mice with LPS-induced ALI. In the LPS-stimulated RAW 264.7 cells, PQ inhibited the release of pro-inflammatory cytokines and increased the mRNA expression of monocyte chemoattractant protein-1 (MCP-1). Treatment with PQ decreased the translocation of nuclear factor (NF)B to the nucleus, and increased the nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2) and the expression of HO-1. PQ also inhibited the activation of p38 in the LPS-stimulated RAW 264.7 cells. Taken together, our findings demonstrate that PQ exerts anti-inflammatory effects against LPS-induced ALI, and that these effects are associated with the modulation of iNOS, HO-1, NFB and MAPK signaling. Therefore, we suggest that PQ has therapeutic potential for use in the treatment of ALI.-
dc.publisherSpandidos Publ Ltd-
dc.titlePicrasma quassiodes (D. Don) Benn. attenuates lipopolysaccharide (LPS)-induced acute lung injury = 소태나무의 LPS-유도 급성폐손상 완화 효과-
dc.title.alternativePicrasma quassiodes (D. Don) Benn. attenuates lipopolysaccharide (LPS)-induced acute lung injury-
dc.typeArticle-
dc.citation.titleInternational Journal of Molecular Medicine-
dc.citation.number0-
dc.citation.endPage844-
dc.citation.startPage834-
dc.citation.volume38-
dc.contributor.affiliatedAuthorJae Won Lee-
dc.contributor.affiliatedAuthorJi Won Park-
dc.contributor.affiliatedAuthorNa Rae Shin-
dc.contributor.affiliatedAuthorSo Yeon Park-
dc.contributor.affiliatedAuthorOk-Kyoung Kwon-
dc.contributor.affiliatedAuthorHyun Ah Park-
dc.contributor.affiliatedAuthorYourim Lim-
dc.contributor.affiliatedAuthorHyung Won Ryu-
dc.contributor.affiliatedAuthorHeung Joo Yuk-
dc.contributor.affiliatedAuthorJung Hee Kim-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.alternativeName이재원-
dc.contributor.alternativeName박지원-
dc.contributor.alternativeName신나래-
dc.contributor.alternativeName박소연-
dc.contributor.alternativeName권옥경-
dc.contributor.alternativeName박현아-
dc.contributor.alternativeName임유림-
dc.contributor.alternativeName류형원-
dc.contributor.alternativeName육흥주-
dc.contributor.alternativeName김정희-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName안경섭-
dc.identifier.bibliographicCitationInternational Journal of Molecular Medicine, vol. 38, pp. 834-844-
dc.identifier.doi10.3892/ijmm.2016.2669-
dc.subject.keywordAcute lung injury-
dc.subject.keywordHeme oxygenase-1-
dc.subject.keywordInducible nitric oxide synthase-
dc.subject.keywordMitogen-activated protein kinase-
dc.subject.keywordNeutrophils-
dc.subject.keywordNuclear factorB-
dc.subject.keywordPicrasma quassiodes (D. Don) Benn.-
dc.subject.localAcute lung injury-
dc.subject.localacute lung injury-
dc.subject.localAcute Lung Injury-
dc.subject.localacute lung injury (ALI)-
dc.subject.localHeme oxygenase-1-
dc.subject.localHeme-oxygenase 1-
dc.subject.localInducible nitric oxide synthase (iNOS)-
dc.subject.localInducible nitric oxide synthase-
dc.subject.localinducible nnitric oxide synthase-
dc.subject.localiNOS-
dc.subject.localInducible nitric oxide synthease (iNOS)-
dc.subject.localINOS-
dc.subject.localinducible nitric oxide synthase-
dc.subject.localmitogen-activated protein kinase-
dc.subject.localMitogen activated protein kinase-
dc.subject.localMitogen-activated protein (MAP) kinase-
dc.subject.localmitogen-activated protein kinases-
dc.subject.localMitogen-activated protein kinase (MAPK)-
dc.subject.localMitogen-activated protein kinase-
dc.subject.localMitogenactivated protein kinase-
dc.subject.localmitogen activated protein kinase-
dc.subject.localMitogen-activated protein kinases (MAPKs)-
dc.subject.localMitogen-acti-vated protein kinase-
dc.subject.localMitogen-activated protein kinases-
dc.subject.localNeutrophils-
dc.subject.localNeutrophil-
dc.subject.localneutrophil-
dc.subject.localneutrophils-
dc.subject.localNuclear factorB-
dc.subject.localPicrasma quassioides (D. Don) Benn-
dc.subject.localPicrasma quassiodes (D. Don) Benn.-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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