The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the National Center for Complementary and Alternative Medicine (NCCAM), the Office of Dietary Supplements (ODS), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) or the National Institutes of Health (NIH).
Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis†
Article first published online: 30 OCT 2006
Copyright © 2006 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 54, Issue 11, pages 3452–3464, November 2006
How to Cite
Funk, J. L., Frye, J. B., Oyarzo, J. N., Kuscuoglu, N., Wilson, J., McCaffrey, G., Stafford, G., Chen, G., Lantz, R. C., Jolad, S. D., Sólyom, A. M., Kiela, P. R. and Timmermann, B. N. (2006), Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis. Arthritis & Rheumatism, 54: 3452–3464. doi: 10.1002/art.22180
- Issue published online: 30 OCT 2006
- Article first published online: 30 OCT 2006
- Manuscript Accepted: 26 JUL 2006
- Manuscript Received: 23 FEB 2006
- NIH (NCCAM and ODS). Grant Number: 5-P50-AT-000474
- NIDDK. Grant Number: 5-R01-DK-067286
Scientific evidence is lacking for the antiarthritic efficacy of turmeric dietary supplements that are being promoted for arthritis treatment. Therefore, we undertook studies to determine the antiarthritic efficacy and mechanism of action of a well-characterized turmeric extract using an animal model of rheumatoid arthritis (RA).
The composition of commercial turmeric dietary supplements was determined by high-performance liquid chromatography. A curcuminoid-containing turmeric extract similar in composition to these supplements was isolated and administered intraperitoneally to female Lewis rats prior to or after the onset of streptococcal cell wall–induced arthritis. Efficacy in preventing joint swelling and destruction was determined clinically, histologically, and by measurement of bone mineral density. Mechanism of action was elucidated by analysis of turmeric's effect on articular transcription factor activation, microarray analysis of articular gene expression, and verification of the physiologic effects of alterations in gene expression.
A turmeric fraction depleted of essential oils profoundly inhibited joint inflammation and periarticular joint destruction in a dose-dependent manner. In vivo treatment prevented local activation of NF-κB and the subsequent expression of NF-κB–regulated genes mediating joint inflammation and destruction, including chemokines, cyclooxygenase 2, and RANKL. Consistent with these findings, inflammatory cell influx, joint levels of prostaglandin E2, and periarticular osteoclast formation were inhibited by turmeric extract treatment.
These translational studies demonstrate in vivo efficacy and identify a mechanism of action for a well-characterized turmeric extract that supports further clinical evaluation of turmeric dietary supplements in the treatment of RA.