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

One hundred one isolates of nutritionally variant streptococci from 97 patients were phenotypically characterized and compared with the type strains of Granulicatella adiacens (formerly Abiotrophia adiacens) (ATCC 49175(T)) Abiotrophia defectiva (ATCC 49176(T)), and Granulicatella elegans (formerly Abiotrophia elegans) (DSM 11693(T)). Of the isolates, 55 and 43 resembled G. adiacens and A. defectiva, respectively, while 3 strains resembled G. elegans. Phenotypic characteristics useful in differentiating between species within the genera Granulicatella and Abiotrophia (G. adiacens, G. elegans, Granulicatella balaenopterae, and A. defectiva) were production of alpha- and beta-galactosidase; production of beta-glucuronidase; hippurate hydrolysis; arginine dihydrolase activity; and acid production from trehalose, sucrose, pullulan, and tagatose. From the reports submitted with the specimens, the clinical diagnosis was endocarditis in 58% of patients and septicemia or bacteremia in 26% of patients.
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PMID:Granulicatella and Abiotrophia species from human clinical specimens. 1157 66

Circulating human neutrophils from patients with severe inflammatory disorders such as erysipelas and sepsis are specifically desensitized to complement factor C5a stimulation but not to stimulation with other stimuli like N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-8 (IL-8), leukotriene B4 (LTB4), or platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). In this study, we raised the question whether factors released from polymorphonuclear leukocytes (PMNs) can specifically down-regulate C5a-dependent neutrophil functions. When neutrophils were preincubated with either neutrophil lysates or neutrophil degranulation supernatants, a complete inhibition of C5a-stimulated beta-glucuronidase release and chemotaxis could be observed, whereas FMLP-, IL-8-, LTB4- or PAF-dependent functions were not affected. Serine protease inhibitors like phenylmethylsulfonyl fluoride, antileukoprotease, or elafin abolished this effect. High-performance liquid chromatography of neutrophil degranulation supernatants revealed pronounced inhibition of C5a-dependent neutrophil functions in fractions exerting elastase or cathepsin G activity, but not in fractions exerting proteinase 3 activity. Using purified human leukocyte elastase (HLE), C5a responses like intracellular calcium influx, beta-glucuronidase release, and chemotaxis were also specifically inhibited. Our experiments show that the release of HLE or cathepsin G from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a. Elastase and cathepsin G may therefore play an important role in the down-regulation of acute inflammation.
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PMID:Human leukocyte elastase and cathepsin G are specific inhibitors of C5a-dependent neutrophil enzyme release and chemotaxis. 1514 22

Synthesis and anti-inflammatory effects of certain furo[3',2':3,4]naphtho[1,2-d]imidazole derivatives 12-18 were studied. These compounds were synthesized from naphtho[1,2-b]furan-4,5-dione (10) which in turn was prepared from the known 2-hydroxy-1,4-naphthoquinone (7) in a one pot reaction. Furo[3',2':3,4]naphtho[1,2-d]imidazole (12) was inactive (IC(50) value of >30 microM) while its 5-phenyl derivative 13, with an IC(50) value of 16.3 and 11.4 microM against lysozyme and beta-glucuronidase release, respectively, was comparable to the positive trifluoperazine. The same potency was observed for 5-furan derivative 16 with an IC(50) value of 19.5 and 11.3 microM against lysozyme and beta-glucuronidase release, respectively. An electron-withdrawing NO(2) substituted on 5-phenyl or 5-furanyl group led to the devoid of activity as in the cases of 14 and 17. Among them, compound 15 exhibited significant inhibitory effects, with an IC(50) value of 7.4 and 5.0 microM against lysozyme and beta-glucuronidase release, respectively. For the LPS-induced NO production, the phenyl derivatives 12-15 were inactive while the nitrofuran counterparts 17 and 18 suppress LPS-induced NO production significantly, with an IC(50) value of 1.5 and 1.3 microM, respectively, which are more active than that of the positive 1400 W. Compounds 16-18 were capable of inhibiting LPS-induced iNOS protein expression at a dose-dependent manner in which compound 18, with an IC(50) of 0.52 microM in the inhibition of iNOS expression, is approximately fivefold more potent than that of the positive 1400 W. In the CLP rat animal model, compound 18 was found to be more active than the positive hydrocortisone in the inhibition of the iNOS mRNA expression in rat lung tissue. The sepsis-induced PGE2 production in rat serum decreased 150% by the pretreatment of 18 in a dose of 10 mg/kg.
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PMID:Furo[3',2':3,4]naphtho[1,2-d]imidazole derivatives as potential inhibitors of inflammatory factors in sepsis. 1969 97


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