Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study is to investigate the effect of asiaticoside on collagen-induced arthritis (CIA). The model of CIA mice was prepared and the change of secondary paw swelling and the arthritis scores were observed. In vitro proliferation of spleen cells was examined using MTT assay. The cell-free protein extracts from the arthritic joints and nonarthritic joints were used for the analysis of protein expression of cyclooxygenase-2 (COX-2). And the level of PGE2 in joints was assayed using PGE2 express EIA kit. The tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels in the serum were measured by ELISA. Histopathological examination was performed by hematoxylin-eosin (HE) stain method. Asiaticoside (10, 20 and 40 mg x kg(-1) x d(-1), 22 d, ig) significantly reduced paw swelling, and decreased the arthritis scores. There was a significant reduction in proliferation of spleen cells of CIA mice treated with asiaticoside as compared with that of untreated CIA mice. COX-2, PGE2, TNF-alpha and IL-6 production in CIA mice were inhibited by asiaticoside. Meanwhile, the pathological examination showed that articular cartilage degeneration with synovial hyperplasia and inflammatory cells infiltration in CIA mice was suppressed by asiaticoside. Its active mechanism may be related to inhibiting proliferation of lymphocyte and reduction of expression of COX-2 and inflammatory cytokines.
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PMID:[Inhibitiory action of asiaiticoside on collagen-induced arthritis in mice]. 1788 51

The citrus flavonoid hesperidin has been reported to possess a wide range of pharmacological properties. We have investigated the preventive and therapeutic effects of hesperidin on the development of adjuvant arthritis (AA), a rat model of rheumatoid arthritis (RA). Freund's complete adjuvant was used to induce AA in rats. Secondary paw swelling, polyarthritis index and histopathological assessment of ankle joints were used to evaluate the effects of hesperidin on AA rats. Concanavalin-A-induced T-lymphocyte proliferation and interleukin (IL)-2 production by splenocytes were measured using the MTT assay. Levels of IL-1, IL-6 and tumour necrosis factor (TNF)-alpha secreted by peritoneal macrophages (PM) were measured by RIA. Intragastric administration of hesperidin significantly attenuated secondary paw swelling and reduced the polyarthritis index of AA rats in a dose-dependent manner. In addition, hesperidin clearly ameliorated the pathological changes in AA rats. Hesperidin also restored the suppression of T-lymphocyte proliferation and IL-2 production, and downregulated production of IL-1, IL-6 and TNF-alpha by PM in AA rats. Our results suggest that hesperidin improves AA by downregulating the function of over-active macrophages and by up-regulating the activities of dysfunctional T lymphocytes. Hesperidin may therefore have therapeutic value for the clinical treatment of RA. Further research is required to clarify the detailed mechanisms of the protective effects of hesperidin on AA.
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PMID:Suppression of adjuvant arthritis by hesperidin in rats and its mechanisms. 1823 70

Vitamin K2 [menaquinone-4 (MK-4)] has been reported to induce apoptosis in hepatocellular carcinoma, leukemia, and MDS cell lines. The effects of MK-4 on the development of arthritis have never been addressed so far. In this study, we investigated the effect of MK-4 upon the proliferation of rheumatoid synovial cells and the development of arthritis in collagen-induced arthritis (CIA). We analyzed the effect of MK-4 on the proliferation of fibroblast-like synoviocytes (FLSs) using the 3-(4,5-demethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The proapoptotic effect of MK-4 upon FLS was investigated with annexin V staining and DNA fragmentation and caspase 3/7 assays. Moreover, we analyzed the effect of MK-4 on the development of CIA in female dark agouti rats. Our results indicated that MK-4 inhibited the proliferation of FLS and the development of CIA in a dose-dependent manner. We concluded that MK-4 may represent a new agent for the treatment of RA in the setting of combination therapy with other disease-modifying antirheumatic drugs.
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PMID:Vitamin K and rheumatoid arthritis. 1848 89

Chrysanthemum is a traditional Chinese medicine used in China to treat inflammatory diseases. The total flavonoids Chrysanthemum indicum (TFC) were extracted from the dried bud of Chrysanthemum indicum. Our previous study had demonstrated that TFC was a new class of effective anti-inflammation, analgesia and immunoloregulation agents. In this study, we established an adjuvant arthritis (AA) model by injection of Freund's Complete Adjuvant (FCA) to investigate the effect of TFC on the apoptosis of synoviocytes in AA Rats. Synoviocytes isolated from knee joint of rats were treated with different doses of TFC in vitro. Synoviocytes proliferation was measured by MTT assay, and DNA fragmentations were evaluated on agarose gel electrophoresis. The levels of caspase-3 cleaved fragments were analyzed by Western blot. The annexin V stain assay was used to explore the inhibition of caspase-3 on the amelioration of synoviocytes apoptosis. The results showed that TFC inhibited the proliferation of synoviocytes. Electrophoresis showed higher ladders of DNA bands in the TFC group. Cleaved fragments of caspase-3 were increased significantly. Furthermore, the apoptotic synoviocytes were markedly decreased by the caspase-3 specific inhibitor. These results suggest that TFC could induce synoviocytes apoptosis and suppress proliferation of synoviocytes in adjuvant-induced arthritis rats.
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PMID:Effect of total flavonoids of Chrysanthemum indicum on the apoptosis of synoviocytes in joint of adjuvant arthritis rats. 1871 67

The aim of the study was to investigate the effects of TGP, an active compound extracted from the roots of Paeonia lactiflora Pall, on the activities of synoviocytes in rats with collagen-induced arthritis (CIA) and its possible mechanisms. CIA was induced in male Sprague-Dawley (SD) rats immunized with chicken type II collagen (CII) in Freund's complete adjuvant (FCA). Synoviocytes proliferation was determined by 3-(4, 5-2dimethylthiazal-2yl) 2, 5-diphenyltetrazoliumbromide (MTT) assay. Tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP) levels in synoviocytes were measured by radioimmunoassay (RIA). E-prostanoid (EP)(2) and EP(4) receptors were analyzed by Western blot analysis. The results showed that TGP significantly inhibited the proliferation of synoviocytes, decreased the production of IL-1, TNF-alpha and PGE(2) and elevated the levels of cAMP. Further study showed that TGP could up-regulate the expression of EP(2) and EP(4). These results indicated that TGP might exert its anti-inflammatory effects through inhibiting the production of pro-inflammatory mediators in synoviocytes of CIA rats, which might be associated with its ability to regulate cAMP-dependent EP(2)/EP(4)-mediated pathway.
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PMID:Effects and mechanisms of total glucosides of paeony on synoviocytes activities in rat collagen-induced arthritis. 1897 27

Litsea coreana Levl., a traditional Chinese medicine, has long been used for its diverse benefits such as detoxification and detumescence. Total flavonoids from Litsea coreana Levl. (TFLC) are the effective fraction of L. coreana. This study was designed to investigate the anti-inflammatory effects and mechanisms of TFLC against Feund's complete adjuvant (FCA)-induced arthritis in rats. Arthritis was evaluated by secondary paw swelling, polyarthritis index, body weight and histopathologic analysis. Con A- or LPS-stimulated splenocyte proliferation and cytokine (IL-1 and IL-2) production were assessed by MTT assay and activated mouse cell proliferation assay, respectively. The results indicate that therapeutic administration of TFLC (50, 100, 200 mg/kg, ig x 12 days) could significantly suppress secondary arthritis in rats with adjuvant-induced arthritis (AA). In vivo, TFLC (50, 100, 200 mg/kg, ig x 12 days) augmented splenocyte proliferation and increased IL-2 production in splenocytes, while reduced IL-1 activity in peritoneal macrophages (PM(Phi)) of AA rats. In vitro, TFLC at concentrations from 0.005 to 50 microg/ml exerted the same immunoregulatory effects on AA rats as those in vivo. In addition, an attractive feature of TFLC lies in its apparent lack of toxicity. These results suggest that TFLC without toxicity has a significant anti-arthritic effect on AA rats which could be associated with its anti-inflammatory and immunomodulatory properties.
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PMID:Preliminary study of total flavonoids from Litsea coreana Levl. on experimental adjuvant-induced arthritis in rats. 1905 56

Superparamagnetic iron oxide nanoparticles (SPIONs) are attractive materials that have been widely used in medicine for diagnostic imaging and therapeutic applications. In our study, SPIONs and the corticosteroid dexamethasone acetate (DXM) are co-encapsulated into PLGA microparticles for the aim of locally treating inflammatory conditions such as arthritis. The magnetic properties conferred by the SPIONs could help to maintain the microparticles in the joint with an external magnet. The aim of this study was to investigate the interaction between magnetic microparticles and human synovial fibroblasts in terms of microparticle uptake (FACS, confocal and optical microscopy), internalization mechanism (Prussian Blue staining, TEM, immunofluorescence), cell toxicity (MTT) and tissue reaction after intra-articular injection (histology). The results show that the microparticles have an excellent biocompatibility with synoviocytes and that they are internalized through a phagocytic process, as demonstrated by fluorescence-activated cell sorting and morphological analyses of cells exposed to microparticles. Histological analysis showed that the prepared microparticles did not induce any inflammatory reaction in the joint. This type of carrier could represent a suitable magnetically retainable intra-articular drug delivery system for treating joint diseases such as arthritis or osteoarthritis.
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PMID:Dexamethasone-containing PLGA superparamagnetic microparticles as carriers for the local treatment of arthritis. 1913 44

Madecassoside (MA), a triterpenoid product isolated from Centella asiatica, has been described to exhibit antioxidant and anti-inflammatory activities. The present study was undertaken to determine whether madecassoside (MA) is efficacious against collagen-induced arthritis (CIA) in mice and its possible mechanisms. DBA/1J mice were immunized with bovine type II collagen and treated with MA (3, 10 and 30 mg/kg d, i.g.) from days 21 to 42 after immunization. Arthritis was evaluated by hind paw swelling, polyarthritis index, and histological examination. In vitro proliferation of spleen cells was examined using 3-[4,5-dimethylthylthiazol-2-yl]-2, 5-diphenyltetrazoliumbromide (MTT) assay. Plasma levels of cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-10 (IL-10) and the expression of prostaglandin E(2) (PGE(2)), cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in synovial tissues were also determined. The results showed that comparing with untreated CIA mice, treated with MA dose-dependently suppressed the clinical arthritis score and joints tissues pathological damage, reduced the proliferation of spleen cells, plasma levels of TNF-alpha and IL-6, synovial tissues PGE(2) production and COX-2 protein expression, however, the expression of COX-1 in synovial tissues did not change and the plasma levels of IL-10 were increased. These results suggest that MA can effectively alleviate inflammatory response on CIA, and anti-inflammatory effects of MA can be attributed, at least partially, to the inhibition of pro-inflammatory mediators, including COX-2 expression, PGE(2) production, TNF-alpha and IL-6 levels and the up-regulation anti-inflammatory molecule IL-10.
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PMID:Madecassoside attenuates inflammatory response on collagen-induced arthritis in DBA/1 mice. 1913 46

Overgrowth of the synovium plays an important role in the pathogenesis of rheumatoid arthritis (RA). Platelet-derived growth factor (PDGF) is one of the most potent mitogenic factors of synovial cells, and imatinib mesylate (imatinib) is a specific inhibitor of the PDGF receptor tyrosine kinase. The aim of this study was to elucidate the anti-rheumatic activity of imatinib. The in vivo effects of imatinib were assessed by evaluating the sequential manifestation of adjuvant-induced arthritis in rats using paw volume and clinical scores. Imatinib was found to inhibit rat adjuvant-induced arthritis, but the inhibitory effects were incomplete. To confirm the mechanism of anti-rheumatic-activity of imatinib, we assessed the in vitro effects of imatinib on the proliferation of RA synovial fibroblast-like cells (RASFs) using a MTT assay. Intracellular signaling of PDGF was evaluated by Western blot analysis. Platelet-derived growth factor was found to induce a significant proliferation of RASFs, while imatinib inhibited PDGF-induced proliferation of RASF. Imatinib also inhibited PDGF-induced phosphorylation of the PDGF receptor and Akt, whereas constitutive activated extracellular signal-regulated kinase was not inhibited by imatinib. In contrast, imatinib did not inhibit transforming growth factor beta- and basic fibroblast growth factor-induced proliferation of RASF. Oral administration of imatinib ameliorated adjuvant-induced arthritis in rats, and it inhibited PDGF-induced RASF proliferation through disruption of the PDGF-R to Akt kinase signaling pathway. Because imatinib cannot inhibit the non-PDGF-dependent proliferation of RASFs, the anti-rheumatic effect of imatinib may be incomplete. The development of inhibitors of RASF proliferation may lead to the successful treatment of RA.
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PMID:Imatinib mesylate inhibited rat adjuvant arthritis and PDGF-dependent growth of synovial fibroblast via interference with the Akt signaling pathway. 1956 28

The present study was designed to investigate the effect of hesperidin on rat adjuvant arthritis (AA) and to elucidate the involvement of synoviocytes in this process. Freund's complete adjuvant was used to induce AA in rats. Secondary paw swelling and the index of immune organs of AA rats were measured. Macrophage-like synoviocytes were separated by the method of collagenase and trypsin digestion. Synoviocyte proliferation was assayed by MTT assay. TNF-alpha, IL-1beta and IL-10 production of synoviocytes were examined with ELISA. The levels of TNF-alpha, IL-1beta, IL-10 mRNA were determined using RT-PCR. It was found that intragastric hesperidin administration (80, 160 mg/kg) significantly inhibited secondary paw swelling and restored the index of immune organs of AA rats. Furthermore, synoviocyte proliferation in AA rats was apparently suppressed after hesperidin treatment, which was accompanied by decreased transcription as well as production of TNF-alpha and IL-1beta from synoviocytes. Hesperidin also markedly increased IL-10 at both protein and transcription levels in AA rats. In aggregate, the above results demonstrate that hesperidin has a therapeutic effect on AA and the mechanisms are partly related to inhibiting synoviocyte activity and modulating inflammatory cytokine production of synoviocytes which play a crucial role in the pathogenesis of AA.
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PMID:Hesperidin suppresses adjuvant arthritis in rats by inhibiting synoviocyte activity. 1958 85


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