β-Ionone attenuates LPS-induced pro-inflammatory mediators such as NO, PGE<sub>2</sub> and TNF-α in BV2 microglial cells via suppression of the NF-κB and MAPK pathway
DC Field | Value | Language |
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dc.contributor.author | Kang, Chang-Hee | - |
dc.contributor.author | Jayasooriya, Rajapaksha Gendara Prasad Tharanga | - |
dc.contributor.author | Choi, Yung Hyun | - |
dc.contributor.author | Moon, Sung-Kwon | - |
dc.contributor.author | Kim, Wun-Jae | - |
dc.contributor.author | Kim, Gi-Young | - |
dc.date.accessioned | 2023-11-28T11:40:46Z | - |
dc.date.available | 2023-11-28T11:40:46Z | - |
dc.date.issued | 2013-03 | - |
dc.identifier.issn | 0887-2333 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/68658 | - |
dc.description.abstract | beta-Ionone, a precursor of carotenoids, possesses a variety of biological properties such as anti-cancerous, anti-mutagenic and anti-microbial activity. Nevertheless, anti-inflammatory effects of beta-ionone remain unknown. In this study, we investigated whether ION attenuates the expression of lipopolysaccharide (LPS)-induced pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E-2 (PGE(2)) and tumor necrosis factor-alpha (TNF-alpha) in BV2 microglia cells. Our data showed that beta-ionone significantly inhibits secretion of NO, PGE(2) and TNF-alpha. beta-Ionone also inhibits the expression of inducible NO synthesis (iNOS), cyclooxygenase-2 (COX-2) and TNF-alpha protein and their mRNA in LPS-stimulated BV2 microglia cells. In addition, beta-ionone significantly reduced DNA-binding activity of nuclear factor-kappa B (NF-kappa B) through suppression of nuclear translocation of p50 and p65. We showed that NF-kappa B inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha. We also found that LPS-induced NF-kappa B activation is significantly regulated through inhibition of Akt phosphorylation in the presence of beta-ionone. Finally, we showed that beta-ionone substantially inhibits the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, p38 and JNK, which are closely related to regulation of pro-inflammatory mediator secretion. Taken together, these data imply that beta-ionone regulates LPS-induced NF-kappa B-dependent inflammatory pathways through suppression of Akt and MAPK activation. (C) 2013 Elsevier Ltd. All rights reserved. | - |
dc.format.extent | 6 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.title | β-Ionone attenuates LPS-induced pro-inflammatory mediators such as NO, PGE<sub>2</sub> and TNF-α in BV2 microglial cells via suppression of the NF-κB and MAPK pathway | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.tiv.2012.12.012 | - |
dc.identifier.bibliographicCitation | TOXICOLOGY IN VITRO, v.27, no.2, pp 782 - 787 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000316642800032 | - |
dc.identifier.scopusid | 2-s2.0-84872421822 | - |
dc.citation.endPage | 787 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 782 | - |
dc.citation.title | TOXICOLOGY IN VITRO | - |
dc.citation.volume | 27 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | beta-Ionone | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Prostaglandin E-2 | - |
dc.subject.keywordAuthor | Tumor necrosis factor-alpha | - |
dc.subject.keywordAuthor | Nuclear factor-kappa B | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordPlus | NITRIC-OXIDE SYNTHASE | - |
dc.subject.keywordPlus | NEURODEGENERATIVE DISEASES | - |
dc.subject.keywordPlus | MAMMARY CARCINOGENESIS | - |
dc.subject.keywordPlus | NERVOUS-SYSTEM | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | LIPOPOLYSACCHARIDE | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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