Login to MyKarger

New to MyKarger? Click here to sign up.

Login with Facebook

Forgot Password? Reset your password

Authors, Editors, Reviewers

For Manuscript Submission, Check or Review Login please go to Submission Websites List.

Submission Websites List

Institutional Login (Shibboleth)

For the academic login, please select your country in the dropdown list. You will be redirected to verify your credentials.

Table of Contents
Vol. 11, No. 2, 2004
Issue release date: March – April
Section title: Original Paper
J Biomed Sci 2004;11:186–199
(DOI:10.1159/000076031)

Glossogyne tenuifolia Acts to Inhibit Inflammatory Mediator Production in a Macrophage Cell Line by Downregulating LPS-Induced NF-κB

Wu M.-J.a · Wang L.a · Ding H.-Y.b · Weng C.-Y.a · Yen J.-H.c
Departments of aBiotechnology and bCosmetic Science, Chia-Nan University of Pharmacy and Science, and cScinoPharm Biotech Ltd, Tainan Science-Based Industrial Park, Tainan, Taiwan, ROC

Do you have an account?

Login Information





Contact Information










I have read the Karger Terms and Conditions and agree.



Login Information





Contact Information










I have read the Karger Terms and Conditions and agree.



To view the fulltext, please log in

To view the pdf, please log in

Buy

  • FullText & PDF
  • Unlimited re-access via MyKarger
  • Unrestricted printing, no saving restrictions for personal use
read more

CHF 38.00 *
EUR 35.00 *
USD 39.00 *

Select

KAB

Buy a Karger Article Bundle (KAB) and profit from a discount!

If you would like to redeem your KAB credit, please log in.


Save over 20% compared to the individual article price.
Learn more

Rent/Cloud

  • Rent for 48h to view
  • Buy Cloud Access for unlimited viewing via different devices
  • Synchronizing in the ReadCube Cloud
  • Printing and saving restrictions apply

Rental: USD 8.50
Cloud: USD 20.00


Select

Subscribe

For eJournal Archive and eJournal Backfiles information please contact service@karger.com

* The final prices may differ from the prices shown due to specifics of VAT rules.

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 06, 2003
Accepted: October 03, 2003
Published online: February 19, 2004
Issue release date: March – April

Number of Print Pages: 14
Number of Figures: 10
Number of Tables: 0

ISSN: 1021-7770 (Print)
eISSN: 1423-0127 (Online)

For additional information: http://www.karger.com/JBS

Abstract

Glossogyne tenuifolia (hsiang-ju) (GT) is a traditional antipyretic herb used in Chinese medicine; however, no information is available to explain its action. The objective of this research was to elucidate the molecular pharmacological activity and the effective components in the ethanol extract of GT. We found that GT had potent anti-inflammatory effects on the lipopolysaccharide (LPS)-activated murine macrophages, RAW264.7. GT downregulated LPS-induced expression of inducible nitric oxide synthase (iNOS) by blocking its transcription. GT also caused a dose-dependent inhibition of the release of prostaglandin E2 by repressing the promoter activity of the inducible cyclooxygenase (COX-2) gene. Moreover, GT exerted a dose-dependent inhibition of the LPS-stimulated release of the proinflammatory cytokines, TNF-α, IL-1β, IL-6, and IL-12. To determine the mechanism by which GT inhibits LPS signaling, we focused on nuclear factor-ĸB (NF-ĸB) activation. Western blot analysis revealed that GT abolished LPS-induced inhibitor-ĸB phosphorylation. The electrophoretic mobility shift assay demonstrated that GT abolished LPS-mediated ĸB DNA binding activity. Moreover, macrophages were transfected with a vector coding for the luciferase reporter gene under the control of NF-ĸB cis-acting elements, and the transfected macrophages showed that the LPS-stimulated luciferase activity was GT-sensitive. These results suggest that GT attenuates inflammatory mediator synthesis of activated macrophages through an NF-ĸB-dependent pathway. The active components of GT were identified as oleanolic acid and luteolin-7-glucoside. Both of these compounds inhibited LPS-stimulated inflammatory mediator production and NF-ĸB activation. We conclude that GT inhibits NF-ĸB-mediated gene expression and downregulates inflammatory mediator production in murine macrophages.

© 2004 National Science Council, ROC and S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 06, 2003
Accepted: October 03, 2003
Published online: February 19, 2004
Issue release date: March – April

Number of Print Pages: 14
Number of Figures: 10
Number of Tables: 0

ISSN: 1021-7770 (Print)
eISSN: 1423-0127 (Online)

For additional information: http://www.karger.com/JBS


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.