pristane/proteinuria

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Resveratrol possesses protective effects in a pristane-induced lupus mouse model.

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BACKGROUND Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease characterized by the production of autoantibodies. To date, no therapy has been found to satisfactorily treat SLE. SIRT1 deficiency results in the development of an autoimmune syndrome in mice, including a high titer

Autoantibodies to ribosomal P antigens with immune complex glomerulonephritis in SJL mice treated with pristane.

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BALB/c ByJ mice develop a lupus-like syndrome characterized by anti-nRNP/Sm and Su autoantibodies and immune complex glomerulonephritis after a single i.p. pristane injection. In contrast, mercuric chloride induces anti-fibrillarin Abs only in SJL and other H-2s mice, and not in BALB/c (H-2d) mice.

Nephritogenic autoantibodies but absence of nephritis in Il-12p35-deficient mice with pristane-induced lupus.

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BACKGROUND There is strong evidence that Th1 cytokines are essential for disease in murine models of lupus. Interleukin-12 (IL-12) is essential for Th1 cell differentiation and induces interferon-gamma (IFN-gamma) production. Paradoxically, it has been suggested that an IL-12 defect drives the

[Experimental study of pristane-induced murine lupus model].

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OBJECTIVE To establish a mouse model of systemic lupus erythematosus(SLE) and to discuss the role of environmental factors in the pathogenesis of SLE. METHODS Thirty 10-week-old female BALB/c mice were divided into the model group and control group. The model mice received a single intraperitoneal

Modulation of the immune response in pristane-induced lupus by expression of activation and inhibitory Fc receptors.

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Altered homeostasis in Fcgamma receptor (FcgammaR) expression has been implicated in the induction of both immune complex-mediated glomerulonephritis and autoantibody production in systemic lupus erythematosus. FcgammaRI and III are required for immune complexes to activate inflammatory cells,

The natural killer T cell ligand alpha-galactosylceramide prevents or promotes pristane-induced lupus in mice.

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Systemic lupus erythematosus is a systemic autoimmune disease characterized by inflammation in organs such as kidneys and presence of autoantibodies against nuclear antigens. We have previously shown that CD1d deficiency in BALB/c mice exacerbates lupus nephritis and autoantibody production induced

Prophylactic effect of resveratrol and piperine on pristane-induced murine model of lupus-like disease.

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Systemic lupus erythematosus is a multisystem autoimmune disease. Apart from usual treatments, approximately 50% of lupus patients use complementary medicine. Resveratrol is a phytoalexin with various pharmacological properties. We hypothesised that prophylactic treatment with resveratrol may

Immunomodulatory Effect of Agave tequilana Evaluated on an Autoimmunity Like-SLE Model Induced in Balb/c Mice with Pristane.

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In this work, the immunomodulatory activity of the acetone extract and the fructans obtained from Agave tequilana were evaluated, on the systemic autoimmunity type-SLE model generated by the administration of 2,6,10,14-tetramethylpentadecane (TMPD, also known as pristane) on Balb/c female mice. The

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.

Annexin A1 as a target for managing murine pristane-induced systemic lupus erythematosus.

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Systemic lupus erythematosus (SLE) is a polygenic pathological disorder which involves multiple organs. Self-specific B cells play a main role in the lupus pathogenesis by generating autoantibodies as well as by serving as important autoantigen-presenting cells. Autoreactive T lymphocytes, on the

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.

Pristane-Accelerated Autoimmune Disease in (SWR X NZB) F1 Mice Leads to Prominent Tubulointerstitial Inflammation and Human Lupus Nephritis-Like Fibrosis.

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Mouse models lupus nephritis (LN) have provided important insights into disease pathogenesis, although none have been able to recapitulate all features of the human disease. Using comprehensive longitudinal analyses, we characterized a novel accelerated mouse model of lupus using pristane treatment

Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus.

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Loss-of-function mutations in the Fas death receptor or its ligand result in a lymphoproliferative syndrome and exacerbate clinical disease in most lupus-prone strains of mice. One exception is mice injected with 2,6,10,14-tetramethylpentadecane (TMPD), a hydrocarbon oil commonly known as pristane,

Role of Lgals9 Deficiency in Attenuating Nephritis and Arthritis in BALB/c Mice in a Pristane-Induced Lupus Model.

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OBJECTIVE In systemic lupus erythematosus (SLE), an autoimmune disease associated with multiple organ involvement, the development of lupus nephritis determines prognosis, and arthritis impairs quality of life. Galectin 9 (Gal-9, Lgals9) is a β-galactoside-binding lectin that has been used for

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