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Effects of triptolide from Radix Tripterygium wilfordii (Leigongteng) on cartilage cytokines and transcription factor NF-κB: a study on induced arthritis in rats

Cheng Xiao1,2 email, Jing Zhou2 email, Yinghui He3 email, Hongwei Jia2 email, Linhua Zhao2 email, Ning Zhao2 email and Aiping Lu2,4 email

Institute of Clinical Medicine Research, China-Japan Friendship Hospital, Beijing 100029, PR China

Institute of Basic Theory, China Academy of Traditional Chinese Medicine, Beijing 100700, PR China

National Pharmaceutical Engineering Centre for Herbal Preparations, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330006, PR China

E-institutes of Shanghai Municipal Education Commission (Shanghai University of Traditional Chinese Medicine), Shanghai 201203, PR China

author email corresponding author email

Chinese Medicine 2009, 4:13doi:10.1186/1749-8546-4-13

Published: 2 July 2009

Abstract

Background

Triptolide, an active compound of Radix Tripterygium wilfordii, is immunosuppressive, cartilage protective and anti-inflammatory both in human and animal studies of various inflammatory and autoimmune diseases, including rheumatoid arthritis, but its therapeutic mechanism remains unclear. The aim of this study is to investigate the effects of triptolide on cartilage cytokines in the CIA model.

Methods

Sprague Dawley rats were immunized with type II collagen and orally administered with triptolide. The arthritic scores and incidence changes of the rats were observed. The expression of TNF-α, IL-6, COX-2 and NF-κB in paw cartilage was studied with immunohistochemical staining.

Results

Triptolide, at both high and low doses, significantly lowered the arthritic scores, delayed the onset of arthritis and lowered the arthritis incidence. Triptolide treatment at both high and low doses lowered the expression of TNF-α, IL-6, COX-2 and NF-κB in paw cartilage in arthritic rats.

Conclusion

Triptolide lowers the arthritic scores, delays the onset of collagen induced arthritis and reduces the expressions of TNF-α, IL-6, NF-κB and COX-2 in paw cartilage in arthritic rats.


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