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Effect of Triptolide on T‐Cell Receptor Beta Variable Gene mRNA Expression in Rats With Collagen‐Induced Arthritis
Author(s) -
Wang Jixi,
Wang Aibing,
Zeng Heqing,
Liu Lantao,
Jiang Wenhao,
Zhu Yongjie,
Xu Yudong
Publication year - 2012
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.22479
Subject(s) - t cell receptor , triptolide , pathogenesis , gene expression , arthritis , rheumatoid arthritis , interleukin 17 , t cell , receptor , immunology , beta (programming language) , microbiology and biotechnology , chemistry , endocrinology , gene , medicine , biology , cytokine , immune system , apoptosis , biochemistry , computer science , programming language
Triptolide (TP) has been used in the treatment of rheumatoid arthritis (RA), but its mechanism of action is not understood. T‐cell activation and associated release of cytokines appear to be major factors in the pathogenesis of RA. The overexpression of T‐cell receptor (TCR) variable gene (V gene) fragments can cause the activation and infiltration of autoreactive T cells. This study examines the effects of TP on rats with collagen‐induced arthritis (CIA). The levels of interleukin‐10 (IL‐10) in the serum were examined with ELISA. Compared to the CIA group, the levels of IL‐10 were greater in the TP treatment group. Real‐time quantitative polymerase chain reaction confirmed that the expression of TCR V beta (BV) 15 and TCR BV19 was increased in the CIA group, whereas in the TP treatment group, the expression was decreased. In this study, TP was found to enhance IL‐10 levels and decrease the expression levels of TCR BV15 and TCR BV19. These changes might help explain the effectiveness of TP in the treatment of RA. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.