論文

査読有り
2011年9月

Inhibitory effects of chalcone glycosides isolated from Brassica rapa L. 'hidabeni' and their synthetic derivatives on LPS-induced NO production in microglia

BIOORGANIC & MEDICINAL CHEMISTRY
  • Hirokazu Hara
  • ,
  • Yoko Nakamura
  • ,
  • Masayuki Ninomiya
  • ,
  • Ryosuke Mochizuki
  • ,
  • Tetsuro Kamiya
  • ,
  • Elias Aizenman
  • ,
  • Mamoru Koketsu
  • ,
  • Tetsuo Adachi

19
18
開始ページ
5559
終了ページ
5568
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bmc.2011.07.036
出版者・発行元
PERGAMON-ELSEVIER SCIENCE LTD

Activation of microglia induces the production of various inflammatory mediators including nitric oxide (NO), leading to neurodegeneration in many central nervous system diseases. In this study, we examined the effects of chalcone glycosides isolated from Brassica rapa L. 'hidabeni' on lipopolysaccharide (LPS)-nduced NO production using rat immortalized microglia HAPI cells. 4'-O-beta-D-Glucopyranosyl-3', 4-dimethoxychalcone (A2) inhibited LPS-induced inducible NO synthase (iNOS) expression and NO production. However, A2 did not affect nuclear factor-kappa B and mitogen-activated protein kinase pathways. The signal transduction and activator of transcription 1 (STAT1), which is activated via production of IFN-beta by LPS, is an important transcription factor responsible for LPS-induced iNOS expression. A2 suppressed LPS-induced phosphorylation and nuclear translocation of STAT1, although it had no effects on LPS-induced IFN-beta expression. These results indicate that the inhibitory effect of A2 is due to the prevention of STAT signaling. Moreover, structure-activity relationship studies on newly synthesized 'hidabeni' chalcone derivatives showed that 4'-O-beta-D-glucopyranosyl-3'-methoxychalcone (A11), which has no functional groups in the B-ring, inhibits LPS-induced NO production more potently than A2. (C) 2011 Elsevier Ltd. All rights reserved.

Web of Science ® 被引用回数 : 13

リンク情報
DOI
https://doi.org/10.1016/j.bmc.2011.07.036
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21856162
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000294711100028&DestApp=WOS_CPL