Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 배옥남 | - |
dc.date.accessioned | 2018-04-17T05:53:17Z | - |
dc.date.available | 2018-04-17T05:53:17Z | - |
dc.date.issued | 2016-08 | - |
dc.identifier.citation | CHEMICO-BIOLOGICAL INTERACTIONS, v. 256, Page. 102-110 | en_US |
dc.identifier.issn | 0009-2797 | - |
dc.identifier.issn | 1872-7786 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S000927971630271X?via%3Dihub | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/68028 | - |
dc.description.abstract | Urgent needs still exist for selective control of excessive inflammation. Despite the therapeutic potential of natural compounds against inflammation-associated chronic conditions, lack of specific molecular targets renders these bioactive compounds difficult for further development. Here we examined the bioactivity of coniferyl aldehyde (CA), a natural phenolic compound found in several dietary substances and medicinal plants, elucidating its efficacy both in vivo and in vitro with underlying molecular mechanisms. IFN-gamma/TNF-alpha-stimulated human keratinocytes and lipopolysaccharide (LPS)-stimulated murine macrophages were used to examine the effect of CA in vitro and to elucidate the underlying mechanisms. In vivo models of phorbol 12-myristate 13-acetate (TPA)-induced ear edema and carrageenan (CRG)-induced paw edema were employed to investigate the topical and systemic anti-inflammatory effects of CA, respectively. CA significantly reduced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in LPS-stimulated macrophages. While nuclear factor kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPKs) pathways, the representative cellular pathways for iNOS induction, were not affected by CA, phosphorylation of Janus kinase 2 (JAK2) and signal Transducers and Activators of Transcription 1 (STAT1) and subsequent nuclear translocation of p-STAT1 were significantly decreased by CA. The effect of CA on JAK2-STAT1-iNOS axis was also observed in human keratinocytes stimulated with IFN-gamma/TNF-alpha. Topical application of CA to mice produced significant protection against TPA-induced ear edema along with suppressed epidermal hyperproliferation and leucocyte infiltration. Systemic administration of CA significantly reduced CRG-induced paw edema in rats, where CRG-induced iNOS expression and STAT1 phosphorylation were decreased by CA. In summary, CA has significant anti-inflammatory properties both in vitro and in vivo, mediated by significant selective inhibition of JAK2-STAT1-iNOS signaling. CA is an attractive novel candidate for treating inflammatory diseases associated with excessive production of NO. (C) 2016 Elsevier Ireland Ltd. All rights reserved. | en_US |
dc.description.sponsorship | This work was supported by grants from the Ministry of Health and Welfare, Republic of Korea (HI14C2180 and HI14C2284). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | ELSEVIER IRELAND LTD | en_US |
dc.subject | Coniferyl aldehyde | en_US |
dc.subject | Anti-inflammatory activity | en_US |
dc.subject | JAK2-STAT1 | en_US |
dc.subject | Nitric oxide | en_US |
dc.subject | NITRIC-OXIDE SYNTHASE | en_US |
dc.subject | NF-KAPPA-B | en_US |
dc.subject | ISCHEMIC BRAIN-INJURY | en_US |
dc.subject | FERULIC ACID | en_US |
dc.subject | RHEUMATOID-ARTHRITIS | en_US |
dc.subject | ANTIOXIDANT ACTIVITY | en_US |
dc.subject | SALVIA-PLEBEIA | en_US |
dc.subject | RAW264.7 CELLS | en_US |
dc.subject | GROWTH-FACTOR | en_US |
dc.subject | ACTIVATION | en_US |
dc.title | Selective inhibition of JAK2/STAT1 signaling and iNOS expression mediates the anti-inflammatory effects of coniferyl aldehyde | en_US |
dc.type | Article | en_US |
dc.relation.volume | 256 | - |
dc.identifier.doi | 10.1016/j.cbi.2016.06.029 | - |
dc.relation.page | 102-110 | - |
dc.relation.journal | CHEMICO-BIOLOGICAL INTERACTIONS | - |
dc.contributor.googleauthor | Akram, Muhammad | - |
dc.contributor.googleauthor | Kim, Kyeong-A | - |
dc.contributor.googleauthor | Kim, Eun-Sun | - |
dc.contributor.googleauthor | Shin, Young-Jun | - |
dc.contributor.googleauthor | Noh, Dabi | - |
dc.contributor.googleauthor | Kim, Eunji | - |
dc.contributor.googleauthor | Kim, Jeong-Hyeon | - |
dc.contributor.googleauthor | Majid, Arshad | - |
dc.contributor.googleauthor | Chang, Sun-Young | - |
dc.contributor.googleauthor | Bae, Ok-Nam | - |
dc.contributor.googleauthor | Kim, Jin-Ki | - |
dc.relation.code | 2016001551 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | onbae | - |
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