Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김희선 | * |
dc.date.accessioned | 2016-08-28T10:08:34Z | - |
dc.date.available | 2016-08-28T10:08:34Z | - |
dc.date.issued | 2013 | * |
dc.identifier.issn | 0006-291X | * |
dc.identifier.other | OAK-9837 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/223503 | - |
dc.description.abstract | Microglial activation plays an important role in neurodegenerative diseases. Thus, controlling microglial activation is considered to be a promising therapeutic target for neurodegenerative diseases. In the present study, we found that lancemaside A, a triterpenoid saponin isolated from Codonopsis lanceolata, inhibited iNOS and proinflammatory cytokines in LPS-stimulated BV2 microglial cells. By analyzing molecular mechanisms underlying the anti-inflammatory effects of lancemaside A, we found that lancemaside A selectively inhibited LPS-induced JNK phosphorylation among the three types of MAP kinases. A JNK-specific inhibitor, SP600125, like lancemaside A, significantly inhibited not only NO, TNF-α, and IL-6 productions, but also NF-κB and AP-1 activities, suggesting that JNK inhibition is largely involved in the anti-inflammatory mechanism of lancemaside A. Interestingly, both the lancemaside A and SP600125 inhibited ROS production by suppressing the expression and/or phosphorylation of NADPH oxidase subunit proteins, such as p47phox, p67phox, and gp91phox. The antioxidant effects of lancemaside A and SP600125 appear to be related with an increase of hemeoxygenase-1 expression by both agents. Finally, we demonstrated the neuroprotective effects of lancemaside A and SP600125 in microglia-neuron coculture systems. Collectively, our data suggest that JNK pathway plays a key role mediating anti-inflammatory effects of lancemaside A in LPS-stimulated microglia. © 2013 Elsevier Inc. | * |
dc.language | English | * |
dc.title | Lancemaside A inhibits microglial activation via modulation of JNK signaling pathway | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 431 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 369 | * |
dc.relation.lastpage | 375 | * |
dc.relation.journaltitle | Biochemical and Biophysical Research Communications | * |
dc.identifier.doi | 10.1016/j.bbrc.2013.01.049 | * |
dc.identifier.wosid | WOS:000315842800001 | * |
dc.identifier.scopusid | 2-s2.0-84873716660 | * |
dc.author.google | Jeong Y.-H. | * |
dc.author.google | Jung J.-S. | * |
dc.author.google | Le T.K.V. | * |
dc.author.google | Kim D.-H. | * |
dc.author.google | Kim H.-S. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.date.modifydate | 20240118140922 | * |