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)

Norathyriol, a xanthone aglycon isolated from Tripterospermum lanceolatum, was demonstrated to reduce the plasma leakage elicited by the passive cutaneous anaphylactic reaction in normal as well as in adrenalectomized mice. Capsaicin pretreatment greatly suppressed the local edema caused by antidromic stimulation of the saphenous nerve. The plasma exudation of neurogenic inflammation was also reduced in mice treated with norathyriol, diphenhydramine and methysergide, but not with indomethacin. Norathyriol, cyproheptadine and diphenhydramine combined with methysergide suppressed the ear edema caused by injection of compound 48/80, bradykinin and substance P into the ear. However, indomethacin did not affect this phlogist-induced edema response. Histamine- and serotonin-induced plasma exudation in ear edema was also reduced by norathyriol. In isolated rat peritoneal mast cell preparations, norathyriol produced a dose-dependent inhibition of histamine and beta-glucuronidase release from mast cells challenged by compound 48/80, bradykinin and substance P. In compound 48/80-pretreated mice, norathyriol at higher concentrations suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine combined with methysergide did. These data indicate that the inhibitory effect of norathyriol on local edema is not due to the release of steroid hormones from the adrenal gland, but is probably partly due to suppression of mast cell degranulation and hence reduce the release of chemical mediators which increase vascular permeability, and partly, at least in higher doses, due to protection of the vasculature from challenge by various mediators.
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PMID:Inhibitory effect of norathyriol, a xanthone from Tripterospermum lanceolatum, on cutaneous plasma extravasation. 751 Nov 7

Polymyxin B-induced hind-paw edema was suppressed by abruquinone A, an isoflavanquinone isolated from Abrus precatorius, in normal as well in adrenalectomized mice. Unlike dexamethasone, abruquinone A did not increase the liver glycogen content in fasting adrenalectomized mice. The volume of exuded plasma was significantly reduced by abruquinone A in neurogenic inflammation, passive cutaneous anaphylactic reaction and compound 48/80-induced ear edema. Histamine-, serotonin-, bradykinin- and substance P-induced plasma extravasation in ear edema was also suppressed by abruquinone A. Abruquinone A, like isoproterenol, significantly reduced the bradykinin- and substance P-induced plasma extravasation in normal as well as in compound 48/80-pretreated mice. In addition, abruquinone A suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine/methysergide did. In the in vitro experiments, abruquinone A suppressed the compound 48/80-induced histamine and beta-glucuronidase released from isolated rat peritoneal mast cell preparations. These results suggest that the anti-inflammatory effect of abruquinone A is mediated partly via the suppression of the release of chemical mediators from mast cells and partly via the prevention of vascular permeability changes caused by mediators. The glucocorticoid activity and the release of glucocorticoid hormones from the adrenal gland are probably not involved.
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PMID:Inhibition of plasma extravasation by abruquinone A, a natural isoflavanquinone isolated from Abrus precatorius. 753 81

Like indomethacin, BW755C, diphenhydramine and methysergide, 2-phenyl-4-quinolone (YT-1) suppressed the polymyxin B-induced hind-paw edema. This inhibitory effect of YT-1 was also demonstrated in adrenalectomized mice. YT-1 inhibited the antidromic stimulation of saphenous nerve-induced plasma leakage in dorsal paw skin and reduced the volume of plasma exudation in PCA reaction. Bradykinin-, substance P- and compound 48/80-induced mouse ear edema was suppressed by YT-1 in a dose-dependent manner. In isolated rat peritoneal mast cells, YT-1 produced a dose-dependent inhibition of bradykinin-, substance P- and compound 48/80-induced histamine and beta-glucuronidase release. YT-1 also reduced the TXB2 formation from PMN leukocytes with IC50 2.0 +/- 0.5 microM, however with little effect on LTB4 formation. Histamine- and serotonin-induced plasma exudation in ear edema were reduced by YT-1. Moreover, the maximal response of ileum contraction caused by histamine and serotonin were also suppressed by YT-1 in a dose-dependent manner. In compound 48/80-pretreatment mice, YT-1 failed to suppress the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine combined with methysergide did. These results indicate that the inhibitory effect of YT-1 on local edema formation is not through the release of steroid hormones from adrenal gland, and is probably by suppressing the release of chemical mediators from mast cells, inhibition of prostaglandins formation, and noncompetitive but selective protection of the vasculature against the histamine- and serotonin-induced plasma extravasation.
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PMID:Suppressive effect of 2-phenyl-4-quinolone (YT-1) on hind-paw edema and cutaneous vascular plasma extravasation in mice. 820 10

A lipid fraction obtained by activity-guided fractionation from the hexane extract of Sideritis javalambrensis was evaluated for anti-inflammatory activity. This fraction significantly inhibited paw oedema induced by carrageenan as well as ear oedema induced by 12-O-tetradecanoylphorbol 13-acetate (TPA) in mice after oral or topical administration, respectively. Quantitation of the specific marker myeloperoxidase (MPO) demonstrated that its topical anti-inflammatory activity was associated with reduction in cell infiltration into inflamed tissues. The lipid fraction significantly decreased leukocyte granular enzyme release (beta-glucuronidase), but failed to inhibit superoxide generation. Histamine release from mast cells was also suppressed in a concentration-dependent manner. In addition, non-toxic concentrations of this fraction reduced nitric oxide (NO) generation in lipopolysaccharide (LPS)-treated J774 macrophages. Taken together, these results suggest that the lipid fraction exerts in vivo anti-inflammatory activity with the partial contribution of inhibitory actions on some inflammatory responses.
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PMID:Anti-Inflammatory properties of a lipid fraction obtained from Sideritis javalambrensis. 1104 Dec 50

Increasing evidence suggests that a continuous release of histamine from mast cells occurs in the airways of asthmatic patients and that histamine may modulate functions of other inflammatory cells such as macrophages. In the present study histamine (10(-9)-10(-6) M) increased in a concentration-dependent fashion the basal release of beta-glucuronidase (EC(50) = 8.2 +/- 3.5 x 10(-9) M) and IL-6 (EC(50) = 9.3 +/- 2.9 x 10(-8) M) from human lung macrophages. Enhancement of beta-glucuronidase release induced by histamine was evident after 30 min and peaked at 90 min, whereas that of IL-6 required 2-6 h of incubation. These effects were reproduced by the H(1) agonist (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)heptane carboxamide but not by the H(2) agonist dimaprit. Furthermore, histamine induced a concentration-dependent increase of intracellular Ca(2+) concentrations ([Ca(2+)](i)) that followed three types of response, one characterized by a rapid increase, a second in which [Ca(2+)](i) displays a slow but progressive increase, and a third characterized by an oscillatory pattern. Histamine-induced beta-glucuronidase and IL-6 release and [Ca(2+)](i) elevation were inhibited by the selective H(1) antagonist fexofenadine (10(-7)-10(-4) M), but not by the H(2) antagonist ranitidine. Inhibition of histamine-induced beta-glucuronidase and IL-6 release by fexofenadine was concentration dependent and displayed the characteristics of a competitive antagonism (K(d) = 89 nM). These data demonstrate that histamine induces exocytosis and IL-6 production from human macrophages by activating H(1) receptor and by increasing [Ca(2+)](i) and they suggest that histamine may play a relevant role in the long-term sustainment of allergic inflammation in the airways.
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PMID:Histamine induces exocytosis and IL-6 production from human lung macrophages through interaction with H1 receptors. 1123 57

Histamine is synthesized and released by human basophils, mast cells, and neurons. Its pleiotropic effects are mediated by the activation of 4 receptors: H(1), H(2), H(3), and H(4). With the advent of selective antagonists (the antihistamines widely used to treat allergic disorders), the H(1)-receptor was the first member of the receptor family to be pharmacologically defined. Increasing evidence indicates that, in addition to exerting immediate vascular and bronchial responses, histamine might modulate the immune reaction by interacting with T cells, macrophages, basophils, eosinophils, and monocytes. We have shown that, in vitro, histamine induces a concentration-dependent release of IL-6 and beta-glucuronidase from macrophages isolated from the human lung parenchyma. These effects are inhibited by fexofenadine, an H(1)-receptor antagonist, but not by ranitidine, an H(2)-receptor antagonist. This observation raises the possibility that long-term treatment with fexofenadine might have beneficial effects on immune dysregulation and tissue damage/remodeling associated with histamine-mediated macrophage activation.
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PMID:The histamine-cytokine network in allergic inflammation. 1453 Jul 93


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