gms | German Medical Science

54. Jahrestagung der Norddeutschen Orthopädenvereinigung e. V.

Norddeutsche Orthopädenvereinigung

16.06. bis 18.06.2005, Hamburg

The anti-inflammatory herbal drug, Devil’s Claw (Harpagophytum procumbens) (Allya®) inhibits TNFα gene expression via blockade of protein kinase Cε and AP-1

Meeting Abstract

  • corresponding author G. McGregor - Pascoe Pharmaceutical Preparations GmbH, Medical Sciences Department, Giessen
  • E. Munoz - Cordoba
  • B. Fiebich - Freiburg
  • A. Zimmermann - Freiburg
  • Y. Ibig - Freiburg
  • S. Orlikowski - Freiburg
  • M. Heinrich - London

Norddeutsche Orthopädenvereinigung. 54. Jahrestagung der Norddeutschen Orthopädenvereinigung e.V.. Hamburg, 16.-18.06.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc05novEP11

The electronic version of this article is the complete one and can be found online at:

Published: June 13, 2005

© 2005 McGregor et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Extracts of the secondary roots of Harpagophytum procumbens (Devil´s Claw) are popular as adjunct treatment of osteoarthritis. The molecular mechanisms of its anti-inflammatory effects are unclear. We describe the effects of an ethanolic Devil´s Claw extract (that is the sole ingredient of the propreitory

drug, Allya®) (DC) on the expression and release of tumour necrosis factor α (TNFα), a key pro-inflammatory cytokine.

Materials and methods

TNFα-gene transcription and -release were quantified by northern blot analysis and ELISA respectively. Using western blot analysis and pharmacological inhibitors, those intracellular signalling pathways that are involved in the stimulated expression of TNFα were investigated in LPS-activated isolated human mononuclear cells and related cell-lines.


DC inhibited LPS-induced TNFα gene expression and release in human monocytes. In the murine monocyte cell-line, RAW 264.7, the extract did not influence NFκB-dependent gene transcription or LPS-induced degradation of IκBα. LPS-induced activation of two mitogen activated protein kinases (MAPK), p38 MAPK and JNK, was also unaffected by DC. DC inhibited LPS-induced PKCε-activation. The transcriptional activation, in LPS-stimulated RAW cells, of AP-1, which is a downstream target of PKCε, was also inhibited by DC.


These novel findings reveal that the traditional herbal drug, Devil´s Claw, exerts its anti-inflammatory effects by inhibiting TNFα gene expression through specific inhibition of the PKCε and AP-1 intracellular pathway. This finding is not only relevant for the anti-inflammatory effect of Devil´s Claw but also for its analgesic effects, since the PKCε and AP-1 pathway is also an intracellular mediator of nociception.