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DC Field | Value | Language |
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dc.citation.endPage | 1738 | - |
dc.citation.number | 12 | - |
dc.citation.startPage | 1726 | - |
dc.citation.title | ARCHIVES OF PHARMACAL RESEARCH | - |
dc.citation.volume | 39 | - |
dc.contributor.author | Min, Gahee | - |
dc.contributor.author | Ku, Sae-Kwang | - |
dc.contributor.author | Park, Mi Seon | - |
dc.contributor.author | Park, Tae Joo | - |
dc.contributor.author | Lee, Hyun-Shik | - |
dc.contributor.author | Bae, Jong-Sup | - |
dc.date.accessioned | 2023-12-21T23:06:39Z | - |
dc.date.available | 2023-12-21T23:06:39Z | - |
dc.date.created | 2016-11-04 | - |
dc.date.issued | 2016-12 | - |
dc.description.abstract | A certain nucleosomal protein-high mobility group box-1 (HMGB1)-has recently been established as a late mediator of sepsis, with a relatively wide therapeutic window for pharmacological intervention. Pelargonidin (PEL) is a well-known red pigment found in plants; it has important biological activities that are potentially beneficial for human health. In the present study, we investigated whether PEL can modulate HMGB1-mediated inflammatory responses in human umbilical vein endothelial cells (HUVECs) and in mice. The anti-inflammatory activities of PEL were determined by measuring permeability, leukocyte adhesion and migration, and activation of pro-inflammatory proteins in HMGB1-activated HUVECs and mice, as well as the beneficial effects of PEL on survival rate in the mouse sepsis model. The data showed that PEL had effectively inhibited lipopolysaccharide (LPS)-induced release of HMGB1 and suppressed HMGB1-mediated septic responses, such as hyperpermeability, adhesion and migration of leukocytes, and expression of cell adhesion molecules. Furthermore, PEL inhibited the HMGB1-mediated production of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6), as well as the activation of nuclear factor-kappa B (NF-kappa B) and extracellular signal-regulated kinases 1 and 2 (ERK1/2). Collectively, these results indicate that PEL could be used to treat various severe vascular inflammatory diseases via the inhibition of the HMGB1 signaling pathway. | - |
dc.identifier.bibliographicCitation | ARCHIVES OF PHARMACAL RESEARCH, v.39, no.12, pp.1726 - 1738 | - |
dc.identifier.doi | 10.1007/s12272-016-0834-5 | - |
dc.identifier.issn | 0253-6269 | - |
dc.identifier.scopusid | 2-s2.0-84992183782 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/21057 | - |
dc.identifier.url | http://link.springer.com/article/10.1007%2Fs12272-016-0834-5 | - |
dc.identifier.wosid | 000391395300013 | - |
dc.language | 영어 | - |
dc.publisher | PHARMACEUTICAL SOC KOREA | - |
dc.title | Anti-septic effects of pelargonidin on HMGB1-induced responses in vitro and in vivo | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal; Pharmacology & Pharmacy | - |
dc.identifier.kciid | ART002173835 | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordAuthor | Pelargonidin | - |
dc.subject.keywordAuthor | HMGB1 | - |
dc.subject.keywordAuthor | Sepsis | - |
dc.subject.keywordAuthor | Inflammation | - |
dc.subject.keywordAuthor | HUVEC | - |
dc.subject.keywordPlus | EXTRACELLULAR-MATRIX PROTEINS | - |
dc.subject.keywordPlus | ENDOTHELIAL-CELL MONOLAYERS | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | PROINFLAMMATORY CYTOKINE | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSES | - |
dc.subject.keywordPlus | ORGAN DYSFUNCTION | - |
dc.subject.keywordPlus | ANIMAL-MODELS | - |
dc.subject.keywordPlus | SEVERE SEPSIS | - |
dc.subject.keywordPlus | THERAPEUTIC TARGET | - |
dc.subject.keywordPlus | LATE MEDIATOR | - |
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