Rheumatoid Arthritis: Xiao C

Lu AP, Wu P, Ju DH, Jia HW, Li S, Xu SJ, Zhao N, Xiao C, Wu H, Teng JR, Li Y, Wang SJ, Zhou GQ, Zhang H, Wang AM. · Institute Of Basic Theory, China Acaemy Of Tradtional Chinese Medicine · Zhongguo Zhong Yao Za Zhi. · Pubmed #15988837 No free full text.

This publication has no abstract.

Xiao C, Zhou J, He Y, Jia H, Zhao L, Zhao N, Lu A. · Institute of Basic Theory, China Academy of Traditional Chinese Medicine, Beijing 100700, PR China. · Chin Med. · Pubmed #19570240 links to  free full text

Abstract: 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-alpha, IL-6, COX-2 and NF-kappaB 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-alpha, IL-6, COX-2 and NF-kappaB 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-alpha, IL-6, NF-kappaB and COX-2 in paw cartilage in arthritic rats.

Callahan LF, Wiley-Exley EK, Mielenz TJ, Brady TJ, Xiao C, Currey SS, Sleath BL, Sloane PD, DeVellis RF, Sniezek J. · Thurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7280, USA. · Prev Chronic Dis. · Pubmed #19288987 links to  free full text

Abstract: INTRODUCTION: Previous studies suggest that people with arthritis have high rates of using complementary and alternative medicine (CAM) approaches for managing their arthritis, in addition to conventional treatments such as prescription medications. However, little is known about the use of CAM by diagnosis, or which forms of CAM are most frequently used by people with arthritis. This study was designed to provide detailed information about use of CAM for symptoms associated with arthritis in patients followed in primary care and specialty clinics in North Carolina. METHODS: Using a cross-sectional design, we drew our sample from primary care (n = 1,077) and specialist (n = 1,063) physician offices. Summary statistics were used to calculate differences within and between diagnostic groups, practice settings, and other characteristics. Logistic regression models clustered at the site level were used to determine the effect of patient characteristics on ever and current use of 9 CAM categories and an overall category of "any use." RESULTS: Most of the participants followed by specialists (90.5%) and a slightly smaller percentage of those in the primary care sample (82.8%) had tried at least 1 complementary therapy for arthritis symptoms. Participants with fibromyalgia used complementary therapies more often than those with rheumatoid arthritis, osteoarthritis, or chronic joint symptoms. More than 50% of patients in both samples used over-the-counter topical pain relievers, more than 25% used meditation or drew on religious or spiritual beliefs, and more than 19% used a chiropractor. Women and participants with higher levels of education were more likely to report current use of alternative therapies. CONCLUSION: Most arthritis patients in both primary care and specialty settings have used CAM for their arthritis symptoms. Health care providers (especially musculoskeletal specialists) should discuss these therapies with all arthritis patients.

Lu C, Xu SJ, Xiao C, Yan XP, Zhao LH, Wang JM, Li S, Lu AP. · Institute of Basic Research in Chinical Medicine, Beijing 100700, China. · Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. · Pubmed #18237535 No free full text.

Abstract: AIM:To explore the differences of the gene expression of CD4(+) lymphocytes between the RF(+) and RF(-) patients with rheumatoid arthritis. METHODS: mRNA of all the CD4(+) lymphocytes samples were extracted and identified. Then they were labeled and hybridized to microarrays. RESULTS: Hierarchical clustering analysis showed there were 55 differential expression genes between the RF(+) and RF(-) patients with rheumatoid arthritis. CONCLUSION: There are differential expression genes between the RF(+) and RF(-) patients and these genes are related to immunoresponse.

Lin N, Liu C, Xiao C, Jia H, Imada K, Wu H, Ito A. · Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, No. 16, Nanxiaojie, Dongzhimennei, Beijing 100700, China. · Biochem Pharmacol. · Pubmed #17097618 No free full text.

Abstract: Chinese herbal remedy Tripterygium wilfordii Hook. f. (TWHF) has been reported to be therapeutically efficacious in the treatment of rheumatoid arthritis (RA), but its in vivo actions have not been clarified. The purpose of this study was to investigate the effects of triptolide, a diterpenoid triepoxide extracted from TWHF, on inflammation and cartilage destruction in collagen-induced arthritis (CIA) model mice. Histological examination demonstrated that triptolide significantly reduced the inflammatory responses and cartilage damage in the joint tissues. Interestingly, triptolide interfered with CIA-augmented expression of matrix metalloproteinases-13 and -3, which are considered to be key enzymes in the pathological destruction of cartilage, and simultaneously augmented CIA-reduced tissue inhibitors of metalloproteinases-1 and -2 expression in the joints. Moreover, triptolide inhibited prostaglandin E(2) production via selective suppression of the production and gene expression of cyclooxygenase (COX)-2, but not COX-1. The levels of interleukin (IL)-1beta, tumor necrosis factor alpha and IL-6 were also decreased by triptolide in the joint tissues and sera as well as the suppression of CIA-mediated expression of their mRNAs in the joints. In addition, triptolide treatment in vivo was able to reduce an abundance of nuclear factor-kappaB, the transcriptional factor closely related to the inflammatory process, in articular cartilage and synovium in CIA mice. These results suggest that triptolide exerts novel chondroprotective and anti-inflammatory effects on RA, and the therapeutic action of TWHF on RA is, in part, due to the triptolide activities.

Xiao C, Zhao LH, Lu C. · Institute of Basic Theory, China Academy of Chinese Medical Sciences, Beijing 100700. · Zhongguo Zhong Xi Yi Jie He Za Zhi. · Pubmed #16970089 No free full text.

Abstract: OBJECTIVE: To explore the differential gene expression of peripheral CD4+ among rheumatoid arthritis (RA) patients of cold or heat syndrome type with or without rheumatoid factor (RF). METHODS: Differential gene expression of peripheral CD4+ lymphocytes purified from fasting venous blood of RA patients and healthy subjects was studied using gene chip technique. RESULTS: There were 55 differential genes between RA patients with and without RF, mainly involving those related with immune response and signal transduction. In patients with RF, 71 differential genes, mainly related with functional metabolism and immune response, and in those without RF, 70 related with functional metabolism were found between patients of cold and heat syndrome type respectively, all of them were not repetitive with the above-mentioned 55, and only 2 were found repetitive between the 70 and the 71 differential genes, mainly involving functional metabolism. CONCLUSION: The differential genes between RA patients with or without RF are different with those between patients of heat and cold syndrome type, suggesting the TCM syndrome classification has its own basis of gene expression profile.

Zhou J, Xiao C, Zhao L, Jia H, Zhao N, Lu C, Yang D, Tang JC, Chan AS, Lu AP. · Institute of Basic Theory, China Academy of Traditional Chinese Medicine, Beijing 100700, China. · Int Immunopharmacol. · Pubmed #16399624 No free full text.

Abstract: Triptolide is a purified component from a traditional Chinese herb Tripterygium wilfordii Hook F. It has been shown to have anti-inflammatory and immunosuppressive activities by its inhibitory effect on T cells. But the effect of triptolide on Peyer's patch cells is unknown. Enteric mucosal immune system, including Peyer's patch, is regarded as one of the sites for inducing immunity tolerance, and this intolerance effect has been used to induce oral tolerance which can considerably reduce arthritis severity in several models of experimental polyarthritis and RA patients. In this study, we investigated the effect of triptolide on the Peyer's patch cells and peripheral lymphocytes in collagen induced arthritis (CIA) in rats. CIA in rat is a widely studied animal model of inflammatory polyarthritis with similarities to rheumatoid arthritis (RA). Our data show that triptolide could lower the arthritic scores and delay the onset of CIA. There are more Peyer's patches in triptolide treated rats than in control rats, while there is no difference in Peyer's patch numbers between CIA rats and triptolide treated rats. In the Peyer's patch, more CD4+ cells are observed in CIA rats, and the numbers of CD4+ cells in triptolide treated rats and control rats are similar. While more CD8+ cells are observed in triptolide treated rats, and the numbers of CD8+ cells in CIA rats and control rats are similar. In periphery, more CD4+ cells and less CD4+ cells in CIA rats and triptolide treated rats are respectively observed. Therefore, the regulation on Peyer's patch might explain some of the immunosuppressive activities of triptolide, and enteric immune response might be actively involved in CIA pathogenesis. It is suggested that the Peyer's patch is one of the primary targets of the immunosuppressive activity of triptolide.