3-nitrotyrosine and 4-benzyl-2-methyl-1-2-4-thiadiazolidine-3-5-dione

3-nitrotyrosine has been researched along with 4-benzyl-2-methyl-1-2-4-thiadiazolidine-3-5-dione* in 1 studies

Other Studies

1 other study(ies) available for 3-nitrotyrosine and 4-benzyl-2-methyl-1-2-4-thiadiazolidine-3-5-dione

Article	Year
Glycogen synthase kinase-3beta inhibition attenuates the degree of arthritis caused by type II collagen in the mouse. Clinical immunology (Orlando, Fla.), 2006, Volume: 120, Issue:1 Recently, glycogen synthase kinase-3 (GSK-3) has being identified as an ubiquitous serine-threonine protein kinase that participates in a multitude of cellular processes and plays an important role in the pathophysiology of a number of diseases. The aim of this study was to investigate the effects of GSK-3beta inhibition on the degree of arthritis caused by type II collagen (CII) in the mouse (collagen-induced arthritis; CIA). Mice developed erosive hind paw arthritis when immunized with CII in an emulsion in complete Freund's adjuvant (CFA). The incidence of CIA was 100% by day 28 in the CII-challenged mice and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone. The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of mice with the GSK-3beta inhibitor TDZD-8 (1 mg/kg/day i.p.) starting at the onset of arthritis (day 25) ameliorated the clinical signs at days 26-35 and improved histological status in the joint and paw. Immunohistochemical analysis for nitrotyrosine, poly(ADP-ribose) (PAR), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) revealed a positive staining in inflamed joints from mice subjected to CIA. The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. Plasma levels of tumor necrosis factor (TNF)-alpha and the joint tissue levels of macrophage inflammatory protein (MIP)-1alpha and MIP-2 were also significantly reduced by GSK-3beta inhibition. These data demonstrate that GSK-3beta inhibition exerts an anti-inflammatory effect during chronic inflammation and is able to ameliorate the tissue damage associated with CIA. Topics: Animals; Arthritis, Experimental; Arthritis, Rheumatoid; Chemokine CCL3; Chemokine CCL4; Chemokine CXCL2; Collagen Type II; Cyclooxygenase 2; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Hindlimb; Interleukin-6; Leukocyte Count; Macrophage Inflammatory Proteins; Mice; Mice, Inbred DBA; Monokines; Nitric Oxide Synthase Type II; Poly(ADP-ribose) Polymerases; Protein Kinase Inhibitors; Radiography; Thiadiazoles; Tumor Necrosis Factor-alpha; Tyrosine	2006

Article

Year

Glycogen synthase kinase-3beta inhibition attenuates the degree of arthritis caused by type II collagen in the mouse.

Clinical immunology (Orlando, Fla.), 2006, Volume: 120, Issue:1

Recently, glycogen synthase kinase-3 (GSK-3) has being identified as an ubiquitous serine-threonine protein kinase that participates in a multitude of cellular processes and plays an important role in the pathophysiology of a number of diseases. The aim of this study was to investigate the effects of GSK-3beta inhibition on the degree of arthritis caused by type II collagen (CII) in the mouse (collagen-induced arthritis; CIA). Mice developed erosive hind paw arthritis when immunized with CII in an emulsion in complete Freund's adjuvant (CFA). The incidence of CIA was 100% by day 28 in the CII-challenged mice and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone. The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of mice with the GSK-3beta inhibitor TDZD-8 (1 mg/kg/day i.p.) starting at the onset of arthritis (day 25) ameliorated the clinical signs at days 26-35 and improved histological status in the joint and paw. Immunohistochemical analysis for nitrotyrosine, poly(ADP-ribose) (PAR), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) revealed a positive staining in inflamed joints from mice subjected to CIA. The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. Plasma levels of tumor necrosis factor (TNF)-alpha and the joint tissue levels of macrophage inflammatory protein (MIP)-1alpha and MIP-2 were also significantly reduced by GSK-3beta inhibition. These data demonstrate that GSK-3beta inhibition exerts an anti-inflammatory effect during chronic inflammation and is able to ameliorate the tissue damage associated with CIA.

Topics: Animals; Arthritis, Experimental; Arthritis, Rheumatoid; Chemokine CCL3; Chemokine CCL4; Chemokine CXCL2; Collagen Type II; Cyclooxygenase 2; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Hindlimb; Interleukin-6; Leukocyte Count; Macrophage Inflammatory Proteins; Mice; Mice, Inbred DBA; Monokines; Nitric Oxide Synthase Type II; Poly(ADP-ribose) Polymerases; Protein Kinase Inhibitors; Radiography; Thiadiazoles; Tumor Necrosis Factor-alpha; Tyrosine

2006