Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 류인균 | * |
dc.date.accessioned | 2016-09-21T01:09:13Z | - |
dc.date.available | 2016-09-21T01:09:13Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 0197-0186 | * |
dc.identifier.other | OAK-19308 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/232235 | - |
dc.description.abstract | In the present study, we synthesized and evaluated the anti-inflammatory effects of three tryptamine (Trm) hybrid compounds, HBU-375, HBU-376 and HBU-379. The Click reaction between the azido-Trm and 2- or 4-propazylated paeonol moiety resulted in HBU-376 and HBU-375, respectively. HBU-379 was generated by hybridizing Trm with propazylated acetyl-syringic acid. HBU-376 and HBU-375 dose-dependently inhibited LPS and caused nitric oxide (NO) generation in BV2 cells, whereas HBU-379 minimally inhibited NO generation, indicating that the paeonol unit plays an important role in the anti-inflammatory effect of Trm hybrid compounds. Although HBU-375 and HBU-376 demonstrated a similar inhibitory effect on LPS-induced NO generation, HBU-376 resulted in less cellular toxicity presumably due to the free phenolic hydroxyl group of paeonol. Therefore, HBU-376 may be a promising anti-inflammatory agent conferring minimal cytotoxicity. HBU-376 significantly and dose-dependently inhibited LPS-induced NO products, NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6, MCP-1 and interleukin-1β mRNA expressions and iNOS and COX-2 protein expressions. However, at the same concentrations, Trm or paeonol individually did not inhibit LPS-mediated production of inflammatory molecules. HBU-376 inhibited both LPS-induced STAT-3 phosphorylation and nuclear factor-kappa B (NF-κB) activation. Furthermore, LPS-mediated DNA binding of c-Rel, p50 and p52 to the NF-κB binding site of the iNOS promoter was inhibited by HBU-376, whereas Trm and paeonol did not inhibit LPS-induced NF-κB activation and DNA binding of c-Rel, p50 and p52. Overall, our data suggest that the Trm-paeonol hybrid compound down-regulates inflammatory responses by inhibiting NF-κB and NF-κB-dependent gene expression. This suggests that it is a potential therapeutic agent for inflammatory diseases of the central nervous system. © 2016 Elsevier Ltd | * |
dc.language | English | * |
dc.publisher | Elsevier Ltd | * |
dc.subject | BV2 | * |
dc.subject | Hybridization | * |
dc.subject | Inflammation | * |
dc.subject | Tryptamine | * |
dc.title | A tryptamine-paeonol hybridization compound inhibits LPS-mediated inflammation in BV2 cells | * |
dc.type | Article | * |
dc.relation.volume | 100 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 35 | * |
dc.relation.lastpage | 43 | * |
dc.relation.journaltitle | Neurochemistry International | * |
dc.identifier.doi | 10.1016/j.neuint.2016.08.010 | * |
dc.identifier.wosid | WOS:000388780300005 | * |
dc.identifier.scopusid | 2-s2.0-84985998105 | * |
dc.author.google | Jung E.-H. | * |
dc.author.google | Hwang J.-S. | * |
dc.author.google | Kwon M.-Y. | * |
dc.author.google | Kim K.-H. | * |
dc.author.google | Cho H. | * |
dc.author.google | Lyoo I.K. | * |
dc.author.google | Shin S. | * |
dc.author.google | Park J.-H. | * |
dc.author.google | Han I.-O. | * |
dc.contributor.scopusid | 류인균(55664289900) | * |
dc.date.modifydate | 20240220114752 | * |