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Sida 1 från 21 resultat
N-acetyl-seryl-aspartyl-lysyl-proline ameliorates the progression of renal dysfunction and fibrosis in WKY rats with established anti-glomerular basement membrane nephritis.
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N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is hydrolyzed by angiotensin-converting enzyme, is a natural regulator of hematopoiesis. Here it is shown that Ac-SDKP inhibits TGF-beta action in mesangial cells. Because TGF-beta is thought to play a pivotal role in the development and
Experimental interstitial renal fibrosis in rats: nephritis induced by N-(3,5-dichlorophenyl)succinimide.
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The nephrotoxic properties of the chemical N-(3,5-dichlorophenyl)-succinimide were investigated in rats with a view to establishing the usefulness of this chemically-induced nephritis as a model of chronic interstitial renal fibrosis. The compound was synthesized and given daily by gastric
Ac-SDKP ameliorates the progression of lupus nephritis in MRL/lpr mice.
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N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is an endogenous tetrapeptide which can inhibit the differentiation, migration and activation of macrophages and suppress the proliferation of fibroblast. This study examined the effects of Ac-SDKP on the progression of lupus nephritis (LN). MRL/lpr
Renal Protective Effects of N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) in Obese Rats on a High-Salt Diet.
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BACKGROUND
Obesity is a public health problem, associated with salt sensitive hypertension, kidney inflammation, and fibrosis. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a tetra peptide with anti-inflammatory and anti-fibrotic properties. However, its effect on preventing kidney damage in
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline: mechanisms of renal protection in mouse model of systemic lupus erythematosus.
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Systemic lupus erythematosus is an autoimmune disease characterized by the development of auto antibodies against a variety of self-antigens and deposition of immune complexes that lead to inflammation, fibrosis, and end-organ damage. Up to 60% of lupus patients develop nephritis and renal
Effect of indomethacin on the synthesis of glomerular basement membrane and on proteinuria in rats with nephrotoxic nephritis.
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The effect of indomethacin on protein excretion and on the synthesis of glomerular basement membrane (GBM) was studied during various stages of nephrotoxic nephritis (NTN) in the rat. Daily administration of indomethacin (4 mg/kg) was instituted 1, 6, or 21 days after the induction of NTN with 210,
Expression and activation of proline-rich tyrosine kinase 2 (PYK2) in peripheral blood mononuclear cells from patients with systemic lupus erythematosus.
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This study analysed the expression and activation of proline-rich tyrosine kinase 2 (PYK2) in peripheral blood mononuclear cells (PBMCs) from 36 systemic lupus erythematosus (SLE) patients and explored whether activation of PYK2 correlates with disease activity or organ damage in SLE. Samples from
Activation signal transduction by proline-rich tyrosine kinase 2 (PYK2) in peripheral blood mononuclear cells from patients with systemic lupus erythematosus.
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To explore the role of proline-rich tyrosine kinase 2 (PYK2) in systemic lupus erythematosus (SLE), we studied the expression, activation, and function of PYK2 in peripheral blood mononuclear cells (PBMC) from 36 SLE patients. As controls, samples from 19 patients with rheumatoid arthritis and 15
Transforming growth factor-beta receptors in self-limited vs. chronic progressive nephritis in rats.
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Increases in transforming growth factor-beta (TGF-beta) expression and extracellular matrix accumulation are transient in acute self-limited mesangial proliferative glomerulonephritis induced by a single injection of anti-thymocyte serum (ATS), while these increases persist following repeated
Nucleosome effects on mesangial cell matrix and proliferation: a possible role in early lupus nephritis.
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BACKGROUND
Oligonucleosomes (ON) have been demonstrated in the circulation and biopsies of lupus nephritis patients. Their presence as immune complexes is an early and persistent finding in lupus nephritis as are changes in mesangial matrix. Since ON competitively bind to glomerular mesangial cells
Biochemical properties of glomerular basement membrane in daunomycin nephrosis and nephrotoxic serum nephritis.
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Glomerular basement membrane (GBM) were isolated from the kidneys of rats suffering from daunomycin nephrosis or nephrotoxic serum nephritis. The GBM from daunomycin nephrotic rats contained significantly less hydroxyproline, hydroxylysine and glycine than that of control rats. There was an increase
Curcumin modulation of the activation of PYK2 in peripheral blood mononuclear cells from patients with lupus nephritis.
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UNASSIGNED
Proline-rich tyrosine kinase 2 (PYK2) provides important signals during the activation of lymphocytes, which is essential in autoimmune diseases. Systemic lupus erythematosus (SLE) is a representative autoimmune disease, and lupus nephritis (LN) is one of its most severe complications.
Functional activation of proline-rich tyrosine kinase2 (PYK2) in peripheral blood mononuclear cells from patients with systemic lupus erythematosus.
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BACKGROUND
Systemic lupus erythematosus (SLE) is a representative systemic autoimmune disease characterized by activated T cells and polyclonally activated B cells that produce autoantibodies. Activation of autoreactive T and B cells plays a pivotal role in the pathogenesis of this disease. A role
C5b-8 and C5b-9 modulate the collagen release of human glomerular epithelial cells.
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Aside from their lytic function the late complement components C5b-9 stimulate release of prostanoids, interleukin 1 and oxygen radicals from a number of cells. Since C5b-9 has also been connected to the development of sclerosis in animal models of glomerulonephritis, we addressed the question
The Potential effect of G915C polymorphism in regulating TGF-β1 transport into Endoplasmic Reticulum for cytokine production.
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The TGF-β1 cytokine concentration is known to be higher in nephritis with implied Lupus Nephritis severity. The production of TGF-β1 cytokine is associated with G915C polymorphism. Therefore, it is of interest to study G915C polymorphism. The G915C polymorphism changes codon 25 which encodes
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