Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0850803 (anaphylaxis)
 8,092 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of aqueous extract of Gleditsia sinensis thorns (Leguminosae) (GSAE) on the mast cell-dependent anaphylaxis. GSAE (0.005 to 1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in rats. GSAE (0.1 and 1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. When GSAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. GSAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP in RPMC, When CSAE (1 mg/ml) was added, transiently and significantly increased about fourfold compared with that of basal cells. Moreover, GSAE (0.01 and 0.1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha production from RPMC. These results suggest a possible use of GSAE in managing mast cell-dependent anaphylaxis.
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PMID:Inhibitory effect of mast cell-dependent anaphylaxis by Gleditsia sinensis. 1097 91

IgE plays a central role in allergic reactions. Some anti-IgE antibodies (HMK-12, 6HD5) inhibit the binding of IgE to the FcepsilonRI of mast cells/basophilic leukemia cells (PT-18, RBL/2H3), but less inhibition is seen with the anti-allotypic JKS-6 and the anti-idiotypic Eb-1. Anti-IgE HMK-12 can detach bound IgE molecules from the FcepsilonRI. When mast cells or basophils were incubated with monoclonal anti-DNP-IgE SPE-7, washed and treated with anti-IgE HMK-12, anti-IgE/IgE complexes were found in the supernatant. Similar results were obtained with the Fab fragment of HMK-12. Mice injected with anti-DNP-IgE SPE-7 and later with DNP-BSA had the typical systemic anaphylactic shock. However, if they were injected with the anti-IgE antibody (HMK-12) before the challenge, they did not get an anaphylactic shock. In the sera of mice injected with monoclonal IgE SPE-7 and anti-IgE antibody (HMK-12), IgE/anti-IgE complexes were detected. No passive cutaneous anaphylaxis occurred if the rats were injected with anti-IgE antibodies before the challenge. In summary, anti-IgE antibodies can remove IgE antibodies from the FcepsilonRI; anti-IgE/IgE complexes can be detected in vitro and in vivo, and anti-IgE antibodies can inhibit IgE-mediated systemic or local anaphylactic reactions.
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PMID:Rat monoclonal anti-murine IgE antibody removes IgE molecules already bound to mast cells or basophilic leukemia cells, resulting in the inhibition of systemic anaphylaxis and passive cutaneous anaphylaxis. 1203 98

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a newly assigned member of the Ig-immunoreceptor tyrosine-based inhibitory motif superfamily, and its functional role is suggested to be an inhibitory receptor that modulates immunoreceptor tyrosine-based activation motif-dependent signaling cascades. In this study, we hypothesized that PECAM-1 plays an essential in vivo role as a counterregulator of immediate hypersensitivity reactions. We found that PECAM-1 was highly expressed on the surface of immature bone marrow mast cells and at a lower density on mature peritoneal mast cells. Examination of skin biopsies from PECAM-1(+/+) and PECAM-1(-/-) mice revealed that absence of PECAM-1 did not affect mast cell development or the capacity of mast cells to populate tissues. To examine whether the absence of PECAM-1 would influence immediate hypersensitivity reactions, PECAM-1(+/+) and PECAM-1(-/-) mice were presensitized with anti-DNP mouse IgE and then challenged 20 h later with DNP-BSA or PBS. PECAM-1(-/-) mice exhibited elevated serum histamine concentrations after Ag stimulation compared with PECAM-1(+/+) mice, indicating an increased severity of systemic IgE-mediated anaphylaxis. PECAM-1(-/-) mice have increased sensitivity to local cutaneous IgE-dependent anaphylaxis compared with PECAM-1(+/+) mice, as assessed by greater tissue swelling of their ears and mast cell degranulation in situ. PECAM-1(-/-) bone marrow mast cells showed enhanced dense granule serotonin release after Fc epsilon RI cross-linking in vitro. These results suggest that PECAM-1 acts as a counterregulator in allergic disease susceptibility and severity and negatively modulates mast cell activation.
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PMID:Absence of platelet endothelial cell adhesion molecule-1 (CD31) leads to increased severity of local and systemic IgE-mediated anaphylaxis and modulation of mast cell activation. 1205 65

The effect of aqueous extract of Salvia plebeia R. Brown (Labiatae) (SPAE) on the mast cell mediated immediate-type allergic reactions in rats was studied. SPAE (0.05 to 1 g/kg) inhibited systemic allergic reaction induced by compound 48/80. SPAE (0.001 and 1 g/kg) dose-dependently inhibited passive cutaneous anaphylaxis (PCA) when intraperitoneally, intraveneously or orally administered. When SPAE was pretreated at the same concentrations with systemic allergic reaction test, the plasma histamine levels were reduced in a dose-dependent manner. SPAE (0.001 to 1 mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP in RPMC, when SPAE (0.1 and 1 mg/mL) was added, significantly increased compared with that of basal cells. Moreover, SPAE (0.01 to 1 mg/mL) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha (TNF-alpha) production. These results indicate that SPAE may possess strong antiallergic activity and suggest that differences in bioavailability may cause differential activity following different administration routes.
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PMID:Inhibition of immediate-type allergic reactions by the aqueous extract of Salvia plebeia. 1206 55

The effect was investigated of the aqueous extract of Rubus coreanus Miq. (Rosaceae) fruits (RCAE) on systemic and local anaphylaxis. RCAE (0.01-1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. RCAE (1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. Pretreatment with RCAE at the same concentration before systemic anaphylaxis reduced the plasma histamine levels in a dose-dependent manner. RCAE (0.001-1 mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMC, when RCAE was added, significantly increased, compared with that of the normal control. Moreover, RCAE (0.01-1 mg/mL) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha production from RPMC. These results indicate that RCAE may possess antianaphylactic action.
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PMID:Action of Rubus coreanus extract on systemic and local anaphylaxis. 1223 5

To evaluate the antithrombotic activities of puerarin and daidzin from the rhizome of Pueraria lobata, in vitro and ex vivo inhibitory activities of these compounds and their metabolite, daidzein, were measured. These compounds inhibited ADP- and collagen-induced platelet aggregation. Daidzein was the most potent. However, when puerarin and daidzin were intraperitoneally administered, their antiaggregation activities were weaker than when these compounds were administered orally. When in vivo antithrombotic activities of these compounds against collagen and epinephrine were measured, these compounds showed significant protection from death due to pulmonary thrombosis in mice. To evaluate the antiallergic activity of puerarin, daidzin, and daidzein, their inhibitory effects on the release of beta-hexosaminidase from RBL 2H3 cells and on the passive cutaneous anaphylaxis (PCA) reaction in mice were examined. Daidzein exhibited potent inhibitory activity on the beta-hexosaminidase release induced by DNP-BSA and potently inhibited the PCA reaction in rats. Daidzein administered intraperitoneally showed the strongest inhibitory activity and significantly inhibited the PCA reaction at doses of 25 and 50mg/kg with inhibitory activity of 37 and 73%, respectively. The inhibitory activity of intraperitoneally administered daidzein was stronger than those of intraperitoneally and orally administered puerarin and daidzin. Therefore we believe that puerarin and daidzin in the rhizome of Pueraria lobata are prodrugs, which have antiallergic and antithrombotic activities, produced by intestinal microflora.
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PMID:Antithrombotic and antiallergic activities of daidzein, a metabolite of puerarin and daidzin produced by human intestinal microflora. 1239 89

The effect of aqueous extract of Phlomis umbrosa Turcz. (Labiatae) root (PUAE) on mast cell-dependent immediate-type allergic reaction by anal therapy was investigated. PUAE (0.01 to 1 g/kg) dose-dependently inhibited systemic anaphylaxis induced by compound 48/80 in mice. When PUAE was pretreated at the same concentrations with systemic anaphylaxis, the plasma histamine levels were reduced in a dose-dependent manner. PUAE (0.1 and 1 g/kg) also significantly inhibited local anaphylaxis activated by anti-DNP IgE. PUAE (0.001 to 1 mg/mL) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. The level of cyclic AMP (cAMP) in human mast cells (HMC-1 cells) when PUAE (1 mg/mL) was added, transiently and significantly increased compared with that of basal cells. In addition, PUAE (0.1 and 1 mg/mL) inhibited the secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-stimulated HMC-1 cells. These results provide evidence that anal therapy of PUAE may be beneficial in the treatment of allergic diseases.
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PMID:Effect of Phlomis umbrosa root on mast cell-dependent immediate-type allergic reactions by anal therapy. 1267 1

We have previously shown that murine IgG1 antibodies comprise two functionally distinct types regarding their ability to induce mast cell degranulation. In this work, we identified two IgG1-producing hybridomas, both with the same antigenic specificity (anti-DNP), but different in vivo anaphylactic activities. Whereas one of them secretes the anaphylactic IgG1 antibody, as assessed by passive cutaneous anaphylaxis, the other produces the non-anaphylactic IgG1 molecule. The evaluation of the ability of both types of IgG1 to bind to and activate a mouse mast cell line revealed that the anaphylactic IgG1 has a higher binding capacity and releases more beta-hexosaminidase from mast cells than the non-anaphylactic IgG1. Aglycosylated IgG1 obtained by treatment of the anaphylactic IgG1-producing hybridoma line with an inhibitor of N-glycosylation failed to elicit anaphylaxis. In addition, a goat anti-mouse IgG1 antibody reacted less with this aglycosylated IgG1 than with the glycosylated form. These results suggest that the anaphylactic activity of IgG1 antibodies is closely related to their structural conformation and the proper N-glycosylation of these molecules. Finally, the difference in the anaphylactic property between the two types of IgG1 seems to be primarily due to binding to the mast cell surface.
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PMID:Anaphylactic and non-anaphylactic murine IgG1 differ in their ability to bind to mast cells: relevance of proper glycosylation of the molecule. 1277 58

In this study, we measured the antiallergic activities of ginsenosides isolated from the root of Panax ginseng ( Araliaceae), and of their metabolites, as produced by human intestinal bacteria. Compound K, which was identified as a main metabolite, had the most potent inhibitory activity on beta-hexosaminidase release from RBL-2H3 cells and on the PCA reaction. The inhibitory activity of compound K was more potent than that of disodium cromoglycate, one of the commercial anti-allergic drugs. This compound demonstrated a membrane stabilizing action on differential scanning calorimetry. However, compound K did not inhibit the activation of hyaluronidase and did not scavenge active oxygen. These results suggest that the antiallergic action of compound K originates from its cell membrane stabilizing activity and that the ginsenosides of ginseng are prodrugs with extensive antiallergic properties. Abbreviations. compound K:20- O-beta- D-glucopyranosyl-20( S)-protopanaxadiol DNP:dinitrophenol DSCG:disodium cromoglycate DPPC:dipalmitoylphosphatidylcholine DPPH:1,1-diphenyl-2-picrylhydrazyl HSA:human serum albumin IC 50 :50% inhibitory concentration EC 50 :50% effective concentration XOD:xanthine oxidase ICR:Institute of Cancer Research PBS:phosphate buffered saline PCA:passive cutaneous anaphylaxis RAW264.7:mouse monocyte leukemiaRBL-2H3: rat basophil leukemia SD:Sprague-Dawley
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PMID:Antiallergic activity of ginseng and its ginsenosides. 1286 69

Dinitrophenyl derivatives of differing molecular weights and degrees of substitution have been contrasted with respect to their ability to elicit immediate type allergic responses and their capacity to induce antibody formation in the guinea pig. In contradistinction to dinitrophenyl-proteins, bis-DNP-lysine and DNP-polylysines (including a 100,000 molecular weight derivative) failed to induce antibody detectable by guinea pig passive cutaneous anaphylaxis. Dinitrophenyl-polylysines evoked urticarial responses non-specifically, but after succinylation were about as effective as dinitrophenyl-proteins in eliciting specific cutaneous reactions. An important factor influencing the effectiveness of bis-DNP-lysine in evoking specific wheal-and-erythema responses is antibody affinity for the dinitrophenyl-lysyl determinant.
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PMID:Polyfunctional dinitrophenyl haptens as reagents for elicitation of immediate type allergic skin responses. 1448 15


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