Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects of administration of urokinase (UK) and trans-4-aminomethylcyclohexane carboxylic acid (t-AMCHA) on the development of experimental rabbit Masugi nephritis. Treatment with 1000 U/kg of UK, 5000 U/kg of UK and 100 mg/kg of t-AMCHA twice a day intravenously was initiated on the 7th and continued for 7 consecutive days. Concomitantly with the nephrotoxin injection, 5000 U/kg of UK was also given twice a day intravenously for 14 days. The administration of 5000 U/kg of UK twice a day for 7 days and 14 days suppressed the increases in BUN values and the decreases in urinary fibrinolytic activity. Fibrin-fibrinogen degradation products (FDP) were detected more frequently in the urine of rabbits given UK than in the control. Immunofluorescence microscopy showed a decrease in intra- and extra-glomerular fibrin deposition, and a decrease in fibrin or fibrinoid deposits in Bowman's space by 5000 U/kg of UK was demonstrated electron microscopically. Light microscopy revealed that the accumulation of fibrin in glomeruli, crescent formation, and progressive glomerular disorganization by 5000 U/kg of UK were prevented. On the other hand, treatment with t-AMCHA enhanced the increase in BUN values and there was a decrease in urinary fibrinolytic activity. Dense fibrin deposits in the glomeruli, were observed immunopathologically by treatment with t-AMCHA and histopathologic changes were found to be even more severe.
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PMID:Effects of fibrinolytic treatment on rabbit Masugi nephritis. 662 55

Effects of heparin, urokinase, and ancrod were concurrently compared on intraglomerular coagulation using a model of progressive Masugi nephritis. Evaluations were performed with light and immunofluorescent microscopy. Treatment significantly reduced crescent formation, more markedly with ancrod. In contrast, endocapillary proliferation was enhanced in the groups treated with urokinase and, especially, ancrod. Ancrod appeared to be most effective in decreasing the glomerular deposition of fibrinogen-related materials as judged from the immunofluorescence, and a relatively high dose was required for urokinase to be comparable with ancrod. However, in some glomeruli from two of 13 animals given ancrod, mesangiolytic lesion developed. Thus, although promising, ancrod has many problems to be solved before using it to control endocapillary proliferation and mesangiolysis.
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PMID:Comparative effects of heparin, urokinase, and ancrod on intraglomerular coagulation induced in progressive Masugi nephritis. 676 Jun 67