Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune synovitis in rabbits was investigated as a potential in vivo model for evaluating new antiinflammatory agents. Antigen-induced increases in knee width as well as beta-glucuronidase and acid phosphatase activities in exudates were observed. Histologically, polymorphonuclear leukocytes appeared within hours in synovial tissues and reached maximum infiltration at about 24 hours. Subsequently, mononuclear cells, including plasma cells, appeared. The 6-hour Arthus-like phase of synovitis can be depressed by some antiinflammatory agents, colchicine and steroids being particularly effective. It is suggested that this model can be utilized to define potentially more effective antiinflammatory drugs.
 ...
PMID:Effects of antiinflammatory agents on the acute response of immune synovitis in rabbits. 87 2

The contribution of neutrophil-derived elastase and cathepsin G to joint pathology has been examined in immune arthritis in the mouse. Neutrophils from beige mice are genetically deficient in lysosomal elastase and cathepsin G, but have normal levels of the acid hydrolases, beta-glucuronidase, and N-acetyl-beta-glucosaminidase. The development of antigen-induced arthritis in normal mice has been compared with that in beige mice. The pattern of synovitis (both leukocyte accumulation and plasma leakage) were indistinguishable in normal and beige mice. Cartilage proteoglycan depletion was quantified by measuring the decrease in safranin O staining intensity, and this, too, was unaltered in mice lacking elastase and cathepsin G. These results suggest that neutrophil elastase and cathepsin G do not contribute to these aspects of joint pathology in antigen-induced arthritis in the mouse.
 ...
PMID:Pathogenesis of antigen-induced arthritis in mice deficient in neutrophil elastase and cathepsin G. 224 Jan 59

Tissue kallikrein is an enzyme that forms the vasoactive peptide kallidin from an endogenous substrate L-kininogen. Tissue kallikrein has been identified in joint fluids and in inflammatory infiltrates within synovial membranes. It is suggested that tissue kallikrein and kinins have an important role in synovitis and joint damage. Immunoreactive tissue kallikrein and amidase activity were both measured in the synovial fluid of 24 patients with rheumatoid arthritis (RA) and 12 with osteoarthritis (OA). Active enzyme concentrations were higher in RA than in OA and correlated well with the lysosomal enzymes beta-glucuronidase and lactate dehydrogenase. Both total immunoreactive tissue kallikrein and the proenzyme values were similar in RA and OA. Tissue kallikrein was localised by immunocytochemistry to the polymorphonuclear leucocytes present in the synovial fluid and membranes of patients with RA.
 ...
PMID:A tissue kallikrein in the synovial fluid of patients with rheumatoid arthritis. 264 23

A novel and very useful technique was developed to assay a lysosomal enzyme released into the joint synovial fluid during zymosan-induced arthritis in mice. This beta-glucuronidase activity correlated with histomorphological changes observed in the joint: vasculitis, synovitis and pannus formation. The antiarthritic drug triamcinolone acetonide improved both biochemical and histological parameters.
 ...
PMID:A novel method for the sampling of synovial fluid in mice. Assay of a synovial lysosomal enzyme in zymosan-induced arthritis. 318 40

Synovitis was induced in rabbits sensitized to bovine serum albumin (BSA) by a modification of the method of Dumonde and Glynn. Agents were administered starting on the day of initial BSA joint challenge and every weekday (14-17 doses) for 17 to 21 day periods. Synovial tissues were then excised and evaluated either (1) histologically for inflammatory cell infiltration, or (2) both histologically and for total IgG, anti-BSA, and beta-glucuronidase levels in homogenates of portions of the same tissues. By the intraperitoneal and oral routes, methylprednisolone (1 mg/kg/day), azathioprine (25-40 mg/kg/day) and cyclophosphamide (10 mg/kg/day) produced significantly decreases of 40-100% in some or all of the parameters measured. Non-steroidal anti-inflammatory drugs, including phenylbutazone, ibuprofen and acetylsalicylic acid at oral doses of 75 or 100 mg/kg/day, were ineffective as were colchicine at 1 mg/kg/day and indomethacin at 5 mg/kg/day. Thus, as we have measured it, this model of rheumatoid arthritis is not affected by those agents considered to be of limited effectiveness in this chronic disease, but is ameliorated by corticoids and some slow acting agents.
 ...
PMID:Chronic immune synovitis in rabbits. II. Modulation by anti-inflammatory and anti-rheumatic agents. 697 4

Immunoglobulin and beta-glucuronidase levels in joint exudates and homogenates of synovial tissues were measured during the course of bovine serum albumin (BSA) antigen-induced synovitis in rabbits. After intra-articular BSA challenge, the anti BSA hemagglutinating antibody in tissue homogenates increased with time up to 14 days. Results obtained indicated relatively greater increases in specific anti-BSA activity compared with total IgG and are compatible with in vivo antibody synthesis by inflamed synovial tissue. beta-Glucuronidase was measured as a reflection of phagocytic cell activity. Tissue enzyme levels increased to a maximum at 1 day and this level persisted up to at least 7 days, despite the fact that exudate enzyme levels reached a maximum at 1 day and then declined significantly over the next 2-3 weeks. These observations reinforce the view that inflamed synovial tissue possesses a substantial potential for perpetuating joint destruction by producing increased levels of inflammatory mediators.
 ...
PMID:Chronic immune synovitis in rabbits. I. Immunoglobulin and beta-glucuronidase analyses of synovial tissues and joint exudates. 734 Apr 64

Spontaneous synovitis developed in the limb joints and rheumatoid factor-like component appeared in the sera of two rabbits from a pool 36 animals in the course of a long-term immunization with bovine nasal cartilage antigens. A single intra-articular injection of proteoglycan antigens regularly provoked a heavy synovitis and cartilage destruction irrespective of whether the booster injections were administered in physiological saline, or in Freund's complete adjuvant. The dose-dependent severity of arthritis suggested that the antibody titre against proteoglycan antigens played an important role in this mechanism. The synovial extract and synovial fluid of knee joints injected with proteoglycan antigens showed an increased enzyme activity concerning the four acid hydrolases (acid phosphatase, cathepsin D, hyaluronidase and beta-glucuronidase). The high activity of lysosomal acid hydrolases which persisted for several months can derange the molecular structure of proteoglycans of cartilage. The degraded proteoglycans may trigger autoimmune reactions, and the process eventually leads to chronic inflammation and joint destruction.
 ...
PMID:Experimental arthritis produced by proteoglycan antigens in rabbits. 745 41