Antagonistic effects of acetylshikonin on LPS-induced NO and PGE(2) production in BV2 microglial cells via inhibition of ROS/PI3K/Akt-mediated NF-kappa B signaling and activation of Nrf2-dependent HO-1
DC Field | Value | Language |
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dc.contributor.author | Jayasooriya, Rajapaksha Gedara Prasad Tharanga | - |
dc.contributor.author | Lee, Kyoung-Tae | - |
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.available | 2019-03-08T16:39:28Z | - |
dc.date.issued | 2015-10 | - |
dc.identifier.issn | 1071-2690 | - |
dc.identifier.issn | 1543-706X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9054 | - |
dc.description.abstract | Although acetylshikonin (ACS) is known to have antioxidant and antitumor activities, whether ACS regulates the expression of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated microglial cells remains unclear. In this study, it was found that ACS isolated from Lithospermum erythrorhizon inhibits LPS-induced nitric oxide (NO) and prostaglandin E-2 (PGE(2)) release by suppressing the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in BV2 microglial cells. Furthermore, ACS reduced the LPS-induced DNA-binding activity of nuclear factor-kappa B (NF-kappa B) and subsequently suppressed iNOS and COX-2 expression. Consistent with these data, ACS attenuated the phosphorylation of PI3K and Akt and suppressed the DNA-binding activity of NF-kappa B by inducing the generation of reactive oxygen species (ROS) in LPS-stimulated cells. In addition, ACS enhanced heme oxygenase-1 (HO-1) expression via nuclear factor-erythroid 2-related factor 2 (Nrf2) activation. Zinc protoporphyrin, a specific HO-1 inhibitor, partially attenuated the antagonistic effects of ACS on LPS-induced NO and PGE(2) production. By contrast, the presence of cobalt protoporphyrin, a specific HO-1 inducer, potently suppressed LPS-induced NO and PGE(2) production. These data indicate that ACS downregulates proinflammatory mediators such as NO and PGE(2) by suppressing PI3K/Akt-dependent NF-kappa B activity induced by ROS as well as inducing Nrf2-dependent HO-1 activity. Taken together, ACS might be a good candidate to regulate LPS-mediated inflammatory diseases. | - |
dc.format.extent | 12 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | SPRINGER | - |
dc.title | Antagonistic effects of acetylshikonin on LPS-induced NO and PGE(2) production in BV2 microglial cells via inhibition of ROS/PI3K/Akt-mediated NF-kappa B signaling and activation of Nrf2-dependent HO-1 | - |
dc.type | Article | - |
dc.identifier.doi | 10.1007/s11626-015-9922-y | - |
dc.identifier.bibliographicCitation | IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL, v.51, no.9, pp 975 - 986 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000363720500014 | - |
dc.identifier.scopusid | 2-s2.0-84945467081 | - |
dc.citation.endPage | 986 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 975 | - |
dc.citation.title | IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL | - |
dc.citation.volume | 51 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Acetylshikonin | - |
dc.subject.keywordAuthor | Nitric oxide | - |
dc.subject.keywordAuthor | Prostaglandin E-2 | - |
dc.subject.keywordAuthor | Nuclear factor-kappa B | - |
dc.subject.keywordAuthor | Heme oxygenase-1 | - |
dc.subject.keywordAuthor | Nuclear factor-erythroid 2-related factor 2 | - |
dc.subject.keywordPlus | ANTIINFLAMMATORY ACTIVITY | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | IMMUNE-RESPONSES | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | REACTIVE OXYGEN | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Developmental Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Developmental Biology | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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