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Inhibitory Effects of GC, an Extract from Herbs, on $TNF-{\alpha}/IL-1{\beta}$-induced Activation of Human Fibroblast-like Sinoviocytes  

Jang Kwang-Ho (Department of Pathology, College of Oriental Medicine, Daejeon University)
Jin Mi-Rim (Department of Pathology, College of Oriental Medicine, Daejeon University)
Park Hee-Ok (Department of Food and Drug, Chosun University)
Kim Dong-Hee (Department of Pathology, College of Oriental Medicine, Daejeon University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.19, no.5, 2005 , pp. 1225-1232 More about this Journal
Abstract
Based on traditional medicine theories, GC, an extract from 5 herbs, has been formulated and prescribed for the treatment of human rheumatoid arthritis(hRA) for many years. The present studies was done to investigate whether GC has inhibitory effects on activation of fibroblast-like sinoviocytes isolated from a RA patient. In tumor necrosis factor-${\alpha}(TNF-{\alpha}$)/ interleukin-IL-$1{\beta}$(IL-$1{\beta}$) treated human sinoviocytes, the mRNA expression of molecular indicators related to pathologic changes of the sinoviocytes were examined using quantitative real-time PCR. The treatment of GC($10{\mu}g/ml$) significantly suppressed the expression of proinflammatory cytokines and chemokines such as $TNF-{\alpha}$, IL-6 and IL-8 compared with the control, but not $IL-1{\beta}$, The mRNA level of intracellular adhesion molecule-1 (ICAM-1) which is known to increase in the activated sinoviocytes of RA patients, was slightly decreased by GC. The expression of NOS-II was considerably reduced, which was accompanied by a decrease in the production of nitric oxide(NO). Furthermore, GC dramatically raised the mRNA levels of tissue inhibitors of matrix metalloproteinase-1 (TIMP-1), while those of matrix metalloproteinase-3 were significantly lowered. Taken together, these data suggested that GC might suppress the activation of sinoviocytes in hRA.
Keywords
GC; hRA; human fibroblast-like sinoviocytes; proinflammatory cytokines; IL-8; ICAM-1; NOS-II; MMP-3; TIMP-1;
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