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Página 1 a partir de 31 resultados
Immune reactivity to connective tissue antigens in pristane induced arthritis.
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OBJECTIVE
Pristane induced arthritis (PIA) is a seropositive experimental murine model that closely resembles rheumatoid arthritis (RA). Immune reactivity to a broad spectrum of autoantigens has been recognized in this disease model. We investigated the specificity of the autoimmune response in PIA
Toll-like receptor 3 upregulation in macrophages participates in the initiation and maintenance of pristane-induced arthritis in rats.
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BACKGROUND
Toll-like receptors (TLRs) are involved in both innate and adaptive immune responses and are likely to play a complex role in the pathogenesis of human rheumatoid arthritis (RA) and experimental arthritis. The objective of this study was to identify the key TLR in pristane-induced
Methotrexate ameliorates pristane-induced arthritis by decreasing IFN-γ and IL-17A expressions.
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OBJECTIVE
This study was carried out to test the effects of methotrexate (MTX) and black seed oil (BSO) on pristane-induced arthritis (PIA) in rats.
METHODS
Inbred dark agouti (DA) rats were induced by a single subcutaneous injection of pristane, and then treated with MTX or BSO. Arthritis severity
A new model of AA-amyloidosis induced by oral pristane in BALB/c mice.
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Fifteen male BALB/c mice were given six intermittent oral doses of O.I. ml pristane (2, 6, 10, 14 tetramethylpentadecane) within a period of 9 weeks. Fifteen mice receiving tap water using the same schedule formed the control group. Amyloidosis was first detected in the spleen of a mouse which had
Therapeutic effect of Withania somnifera on pristane-induced model of SLE.
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Systemic lupus erythematosus commonly known as lupus is an intricate disorder with multiple organ involvement characterized primarily by inflammation caused due to deposition of immune-complexes formed by production of autoantibodies against nuclear, nucleolar as well as cytoplasmic self-antigens.
Oxidative stress and immune complexes: Pathogenic mechanisms in pristane induced murine model of lupus.
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Systemic lupus erythematosus is a systemic autoimmune inflammatory disease with a broad spectrum of clinical presentations. Mouse models play an indispensible role in understanding the disease pathology and for developing new therapeutics. This study investigated the effect of pristane
A novel NF-κB inhibitor, DHMEQ, ameliorates pristane-induced lupus in mice.
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Nuclear factor (NF)-κB is strongly associated with the development of immune regulation and inflammation. The aim of the present study was to identify whether a NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), ameliorates systemic lupus erythematosus (SLE) in a pristane-induced mouse model.
Characterization of pristane-induced arthritis, a murine model of chronic disease: response to antirheumatic agents, expression of joint cytokines, and immunopathology.
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OBJECTIVE
To characterize chronic murine pristane-induced arthritis (PIA) with regard to the response to antirheumatic agents, expression levels of proinflammatory cytokines, and immunopathologic features.
METHODS
Male DBA/1 mice were injected intraperitoneally with pristane oil to induce a chronic
MicroRNA-26a negatively regulates toll-like receptor 3 expression of rat macrophages and ameliorates pristane induced arthritis in rats.
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BACKGROUND
Abnormal toll-like receptor (TLR)3 signaling plays an indispensable role in pathogenesis of both experimental and human rheumatoid arthritis, and microRNAs (miRNAs) might orchestrate this signaling pathway. This study was performed to determine the relationship between miR-26a and TLR3 in
Mechanisms of tumor necrosis factor α antagonist-induced lupus in a murine model.
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OBJECTIVE
Tumor necrosis factor α (TNFα) antagonists are effective for treating rheumatoid arthritis and other inflammatory diseases, but their use can be complicated by the development of lupus-like phenomena. This study was undertaken to investigate the role of TNFα in a murine model of
Toll-like receptor 7-stimulated tumor necrosis factor α causes bone marrow damage in systemic lupus erythematosus.
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OBJECTIVE
To define the pathogenesis of bone marrow (BM) involvement in systemic lupus erythematosus (SLE).
METHODS
Tumor necrosis factor α (TNFα) levels, cell death, and cellular damage in BM from SLE patients, controls, and mice with pristane-induced lupus were analyzed using a morphometric
Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane.
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Interleukin (IL)-17A is increased both in serum and in kidney biopsies from patients with lupus nephritis, but direct evidence of pathogenicity is less well established. Administration of pristane to genetically intact mice results in the production of autoantibodies and proliferative
Prostaglandin E2 receptors EP2 and EP4 are up-regulated in peritoneal macrophages and joints of pristane-treated mice and modulate TNF-alpha and IL-6 production.
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Prostaglandin E(2) (PGE(2)) can have pro- or anti-inflammatory effects, depending on engagement of different PGE(2) receptor (EP) subtypes. The role of EPs in regulating autoimmune inflammation was studied in the murine arthritis/lupus model induced by pristane. Peritoneal macrophages were isolated
Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis.
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BACKGROUND
Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus. As murine models of LN are valuable tools to better understand its pathophysiology and to search for new effective treatments, we investigated the effects of the bioflavonoid quercetin on
Immmunopathogenesis of rheumatoid arthritis; induction of arthritogenic autoimmune responses by proinflammatory stimuli.
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Rheumatoid arthritis (RA) is a severe autoimmune disorder of unknown etiology. Major autoantigens include immunoglobulin G (which is targeted by rheumatoid factor), citrullinated proteins, and the heterogeneous nuclear ribonucleoprotein (hnRNP) A2. To obtain more insight into the pathogenic role of
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