Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jayasooriya, Rajapaksha Gedara Prasad Tharanga | - |
dc.contributor.author | Lee, Kyoung-Tae | - |
dc.contributor.author | Lee, Hak-Ju | - |
dc.contributor.author | Choi, Yung Hyun | - |
dc.contributor.author | Jeong, Jin-Woo | - |
dc.contributor.author | Kim, Gi-Young | - |
dc.date.available | 2017-07-11T05:26:57Z | - |
dc.date.created | 2017-04-10 | - |
dc.date.issued | 2014-03 | - |
dc.identifier.issn | 0278-6915 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11750/2666 | - |
dc.description.abstract | In the present study, we investigated whether β-hydroxyisovalerylshikonin (β-HIVS) affects the production of proinflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) in BV2 microglial cells. Our data showed that β-HIVS inhibited secretion of NO and PGE2 and downregulated expression of their main regulatory genes, inducible NO synthesis (iNOS) and cyclooxygenase-2 (COX-2). β-HIVS also reduced the LPS-induced DNA-binding activity of nuclear factor-κB (NF-κB) by suppressing nuclear translocation of the NF-κB subunits and inhibiting the degradation and phosphorylation of IκBα. Furthermore, an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), attenuated LPS-stimulated iNOS and COX-2 expression, suggesting that NF-κB inhibition is a main effector in the expression of iNOS and COX-2. We also found that LPS-induced NF-κB activation is regulated through inhibition of PI3K/Akt phosphorylation in response to β-HIVS. Additionally, β-HIVS caused the induction of heme oxygenase-1 (HO-1) via upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2), both of which are involved in the secretion of proinflammatory mediators such as NO and PGE2. Taken together, our data indicate that β-HIVS diminishes the proinflammatory mediators NO and PGE2 and the expression of their regulatory genes, iNOS and COX-2, in LPS-stimulated BV2 microglial cells by inhibiting PI3K/Akt-dependent NF-κB activation and inducing Nrf2-mediated HO-1 expression. © 2013 Elsevier Ltd. | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.title | Anti-inflammatory effects of beta-hydroxyisovalerylshikonin in BV2 microglia are mediated through suppression of the PI3K/Akt/NF-kB pathway and activation of the Nrf2/HO-1 pathway | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.fct.2013.12.011 | - |
dc.identifier.scopusid | 2-s2.0-84892170770 | - |
dc.identifier.bibliographicCitation | Food and Chemical Toxicology, v.65, pp.82 - 89 | - |
dc.subject.keywordAuthor | beta-Hydroxyisovalerylshikonin | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Prostaglandin E2 | - |
dc.subject.keywordAuthor | Nuclear factor-kappa B | - |
dc.subject.keywordAuthor | Home oxygenase-1 | - |
dc.subject.keywordAuthor | Nuclear factor-erythroid 2-related factor 2 | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | NITRIC-OXIDE | - |
dc.subject.keywordPlus | HEME OXYGENASE-1 | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | MACROPHAGES | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | SYNTHASE | - |
dc.subject.keywordPlus | CANCER | - |
dc.citation.endPage | 89 | - |
dc.citation.startPage | 82 | - |
dc.citation.title | Food and Chemical Toxicology | - |
dc.citation.volume | 65 | - |
There are no files associated with this item.