頁 1 從 31 結果
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
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
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
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
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.
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
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.
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
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
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
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
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 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
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
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