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      Effects of Xinfeng Capsules on Expression of Platelet Granule Membrane Protein 140 and Platelet Cluster of Differentiation 40 Ligand in Peripheral Blood of Adjuvant Arthritis Rats

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      1 , 2 , *
      International Journal of Rheumatology
      Hindawi Publishing Corporation

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          Abstract

          Platelet GMP-140 and CD40L as specific markers of platelet activation play an important role in the morbidity and development of rheumatoid arthritis. The expression of GMP-140, CD40L increases in peripheral blood of AA rats. And they have correlation with voix pedis' swelling, AI. XFC could inhibit the inflammatory response through inhibiting platelet activation of AA rats, which means decreasing the expression of GMP-140, CD40L in peripheral blood. So, the voix pedis' swelling and AI were decreased as the result.

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          T-cell-mediated signalling in immune, inflammatory and angiogenic processes: the cascade of events leading to inflammatory diseases.

          In the last decade, the understanding of the molecular mechanisms of regulation of the inflammatory process in chronic inflammatory diseases has moved remarkably forward. Recent evidence in various fields has consistently indicated that T-cells play a key role in initiating and perpetuating inflammation, not only via the production of soluble mediators but also via cell/cell contact interactions with a variety of cell types through membrane receptors and their ligands. Signalling through CD40 and CD40 ligand is a versatile pathway that is potently involved in all these processes. In this article, we review how T-cells become activated by dendritic cells or inflammatory cytokines, and how these T-cells activate, in turn, monocytes/macrophages, endothelial cells, smooth muscle cells and fibroblasts to produce pro-inflammatory cytokines (tumour necrosis factor alpha, interleukin-6), chemokines (interleukin-8, monocyte chemotactic protein-1), tissue factor, the main initiator of the coagulation cascade in vivo, and finally matrix metalloproteinases, responsible for tissue destruction. Moreover, we discuss how CD40 ligand at inflammatory sites stimulates fibroblasts and tissue monocyte/macrophage production of VEGF, leading to angiogenesis, which promotes and maintains the chronic inflammatory process. This cascade of events is discussed in the context of disease initiation/progression, with particular reference to atherosclerosis and rheumatoid arthritis, and to potential novel therapeutic targets for their treatment.
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            Increased platelet activation markers in rheumatoid arthritis: are they related with subclinical atherosclerosis?

            Atherosclerotic cardiovascular mortality is increased in rheumatoid arthritis (RA) patients. We evaluated the association of inflammatory response with platelet, endothelial, coagulation activation parameters; and subclinical atherosclerosis in RA patients. We included 27 RA patients (21 female; six male) and 19 healthy subjects (14 female; five male). Disease activity score (DAS28) in RA patients was calculated; and patients were divided into two groups as active and inactive. Flow cytometry was used to determine platelet CD62P expression, platelet microparticles (PMP), platelet-monocyte (PMC) and platelet-neutrophil complexes (PNC). Plasma E-selectin, thrombin-antithrombin (TAT) complex, and serum sCD40L levels were determined by ELISA. The intima-media thickness (IMT) of carotid arteries was determined by B-mode ultrasonography. In RA patients, platelet CD62P expression (p 0.05).The increase in markers of active platelets, CD62P and sCD40L, and PMC levels might be associated with the increased cardiovascular mortality in RA. Nevertheless, none of these parameters were associated with carotid IMT: this suggests that one cross-sectional value might not be a good marker for atherosclerosis
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              The significance of platelet activation in rheumatoid arthritis.

              We evaluated the significance of platelet activation in patients with rheumatoid arthritis (RA). The expression of CD62P and CD63 by platelets was determined using flow cytometry in 18 active RA patients, 10 remission RA and 15 normal controls. Meanwhile, the erythrocyte sedimentation rate (ESR) and C-reactive protein was also determined in all groups. The expression of CD62P in active RA patients (11.88 +/- 2.47%) was significantly higher than that in remission RA group (2.85 +/- 1.60%; P < 0.01) and control group (2.78 +/- 1.04%; P < 0.01). The expression of CD63 in active RA patients (9.90 +/- 3.02%) was significantly higher than that in remission RA group (4.11 +/- 2.00%; P < 0.01) and control group (4.13 +/- 1.85%; P < 0.01). The level of CRP (54.33 +/- 23.35 mg/l) and ESR (86.06 +/- 33.67 mm/h) in active RA patients was higher than that in remission RA group (2.55 +/- 1.01 mg/l, 14.70 +/- 4.57 mm/h; P < 0.01 for both) and normal control group (3.21 +/- 2.18 mg/l, 12.25 +/- 5.05 mm/h; P < 0.01 for both). There was a positive correlation between CD62P and ESR (r = 0.5224, P < 0.01) and also a positive correlation between CD62P and CRP (r = 0.7048, P < 0.01) as well as between CD63 and ESR (r = 0.4476, P < 0.05) but no correlation between CD63 and CRP. Platelet activation may be a sign of RA exacerbation.
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                Author and article information

                Journal
                Int J Rheumatol
                Int J Rheumatol
                IJR
                International Journal of Rheumatology
                Hindawi Publishing Corporation
                1687-9260
                1687-9279
                2012
                7 May 2012
                : 2012
                : 139696
                Affiliations
                1Hubei University of Traditional Chinese Medicine, Hubei, Wuhan 430065, China
                2Department of Rheumatism and Immunity, The First Hospital Affiliated to Anhui College of Traditional Chinese Medicine, Anhui, Hefei 230031, China
                Author notes

                Academic Editor: Ruben Burgos-Vargas

                Article
                10.1155/2012/139696
                3352581
                22611405
                56874995-7fe3-4266-95c7-8e0e36cca013
                Copyright © 2012 Z. Rui-kai and L. Jian.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 25 December 2011
                : 6 February 2012
                Categories
                Research Article

                Rheumatology
                Rheumatology

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