Anti-inflammatory mechanism of ginsenoside Rh1 in lipopolysaccharide-stimulated microglia: critical role of the protein kinase A pathway and hemeoxygenase-1 expression
DC Field | Value | Language |
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dc.contributor.author | Jung, Ji-Sun | - |
dc.contributor.author | Shin, Jin A. | - |
dc.contributor.author | Park, Eun-Mi | - |
dc.contributor.author | Lee, Jung-Eun | - |
dc.contributor.author | Kang, Young-Sook | - |
dc.contributor.author | Min, Sung-Won | - |
dc.contributor.author | Kim, Dong-Hyun | - |
dc.contributor.author | Hyun, Jin-Won | - |
dc.contributor.author | Shin, Chan-Young | - |
dc.contributor.author | Kim, Hee-Sun | - |
dc.date.available | 2021-02-22T13:46:11Z | - |
dc.date.issued | 2010-12 | - |
dc.identifier.issn | 0022-3042 | - |
dc.identifier.issn | 1471-4159 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13085 | - |
dc.description.abstract | P>Microglia activation plays a pivotal role in neurodegenerative diseases, and thus controlling microglial activation has been suggested as a promising therapeutic strategy for neurodegenerative diseases. In the present study, we showed that ginsenoside Rh1 inhibited inducible nitric oxide synthase, cyclooxygenase-2, and pro-inflammatory cytokine expression in lipopolysaccharide (LPS)-stimulated microglia, while Rh1 increased anti-inflammatory IL-10 and hemeoxygenase-1 (HO-1) expression. Suppression of microglial activation by Rh1 was also observed in the mouse brain following treatment with LPS. Subsequent mechanistic studies revealed that Rh1 inhibited LPS-induced MAPK phosphorylation and nuclear factor-kappa B (NF-kappa B)-mediated transcription without affecting NF-kappa B DNA binding. As the increase of pCREB (cAMP responsive element-binding protein) is known to result in suppression of NF-kappa B-mediated transcription, we examined whether Rh1 increased pCREB levels. As expected, Rh1 increased pCREB, which was shown to be related to the anti-inflammatory effect of Rh1 because pre-treatment with protein kinase A inhibitors attenuated the Rh1-mediated inhibition of nitric oxide production and the up-regulation of IL-10 and HO-1. Furthermore, treatment of HO-1 shRNA attenuated Rh1-mediated inhibition of nitric oxide and reactive oxygen species production. Through this study, we have demonstrated that protein kinase A and its downstream effector, HO-1, play a critical role in the anti-inflammatory mechanism of Rh1 by modulating pro- and anti-inflammatory molecules in activated microglia. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | Anti-inflammatory mechanism of ginsenoside Rh1 in lipopolysaccharide-stimulated microglia: critical role of the protein kinase A pathway and hemeoxygenase-1 expression | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/j.1471-4159.2010.07075.x | - |
dc.identifier.scopusid | 2-s2.0-78649993974 | - |
dc.identifier.wosid | 000284852600032 | - |
dc.identifier.bibliographicCitation | JOURNAL OF NEUROCHEMISTRY, v.115, no.6, pp 1668 - 1680 | - |
dc.citation.title | JOURNAL OF NEUROCHEMISTRY | - |
dc.citation.volume | 115 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1668 | - |
dc.citation.endPage | 1680 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.subject.keywordPlus | NITRIC-OXIDE SYNTHASE | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | HEME OXYGENASE-1 | - |
dc.subject.keywordPlus | SUBSTANTIA-NIGRA | - |
dc.subject.keywordPlus | RG1 PROTECTS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | CAMP | - |
dc.subject.keywordPlus | NEUROINFLAMMATION | - |
dc.subject.keywordPlus | PHARMACOKINETICS | - |
dc.subject.keywordAuthor | CREB | - |
dc.subject.keywordAuthor | ginsenoside Rh1 | - |
dc.subject.keywordAuthor | HO-1 | - |
dc.subject.keywordAuthor | neuroinflammation | - |
dc.subject.keywordAuthor | PKA | - |
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