gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie
72. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 94. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie und 49. Tagung des Berufsverbandes der Fachärzte für Orthopädie und Unfallchirurgie

22. - 25.10.2008, Berlin

Antirheumatic effect of Sulforaphan

Meeting Abstract

  • C. Wruck - RWTH Aachen Institut für Anatomie und Zellbiologie, Aachen, Germany
  • M. Kadyrow - RWTH Aachen Institut für Anatomie und Zellbiologie, Aachen, Germany
  • D. Varoga - Christian-Albrecht-Univ. Kiel, Anatomisches Institut, Kiel, Germany
  • M. Tohidnezhad - RWTH Aachen Institut für Anatomie und Zellbiologie, Aachen, Germany
  • L.-O. Brandenburg - RWTH Aachen Institut für Anatomie und Zellbiologie, Aachen, Germany
  • T. Pufe - RWTH Aachen Institut für Anatomie und Zellbiologie, Anatomisches Institut, Aachen, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie. 72. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 94. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 49. Tagung des Berufsverbandes der Fachärzte für Orthopädie. Berlin, 22.-25.10.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocPO12-1292

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dkou2008/08dkou649.shtml

Published: October 16, 2008

© 2008 Wruck et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Objective: Rheumatoid arthritis (RA) is a chronic inflammatory disease in which the synovial environment is characterized by intense immunological activity. We investigated whether sulforaphane (SF) could inhibit the expression of interleukin 6 (IL-6), and IL-1 as well as cell proliferation induced by tumor necrosis factor-α (TNF α) in human immortalised fibroblast-like synoviocytes (FLS).

Methods: FLS were cultured with or without SF. Cytokine and VEGF secretion levels were detected using ELISA. Cell proliferation of FLS induced by TNF-α was determined by Cyquant. NFκB and AP-1 activity was measured by Dual-Luciferase-Assay.

Results: ELISA and promoter-studies analysis revealed that the activity of NFκB and AP-1 and the levels of IL-6, and IL-1 secretion by FLS were reduced by SF in a dose-dependent manner. Cyquant assay showed that SF could inhibit proliferation of FLS induced by TNF-α.

Conclusion: Our results demonstrate that SF inhibits “pro-inflammatory”- transcription factors and -cytokines in FLS. In addition, it reduces TNF-α induced FLS cell proliferation. These findings indicate that treatment of RA-patients with SF might be considered as a new therapeutic strategy to combat joint destruction and inflammation in RA.