共查询到20条相似文献,搜索用时 31 毫秒
1.
Triton X-100 at concentrations preceding those which liberated histamine, produced dose-dependent inhibition of compound 48/80-induced histamine release from rat mast cells. Triton X-100 (0.00002 1/1) depleted ATP content in the mast cells and blocked compound 48/80-induced histamine release. The inhibition of compound 48/80-induced histamine release and depletion of the ATP content in the mast cells was reversed by glucose (10 mmole). It is concluded that inhibition by Triton X-100 of histamine release induced by compound 48/80 is dependent on inhibition of energy production. 相似文献
2.
R G Coffey 《Life sciences》1973,13(8):1117-1130
Lysosomal cationic proteins which release histamine from rat peritoneal mast cells were prepared from circulating as well as peritoneal leukocytes of rabbits. The release of histamine by cationic proteins and by compound was compared as a function of temperature, pH and concentration. Cationic protein-mediated histamine release appears to be a non-cytotoxic energy requiring process similar to compound . It was inhibited by iodoacetate, n-ethylmaleimide, 2,4-dinitrophenol, malonate, oxamate, glutamate and slightly inhibited by 2-deoxyglucose. Pharmacologic inhibition of release by isoproterenol, aminophylline, dibutyryl cyclic AMP and prednisone was also demonstrated. 相似文献
3.
Ward R. Rice Jeffrey A. Whitsett 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1984,805(3):261-267
Release of [3H]phosphatidylcholine from pulmonary Type II epithelial cells was stimulated by terbutaline, forskolin and cytochalasin D. Compound inhibited both basal and agonist-stimulated release of [3H]PC. The IC50 for inhibition by compound was 1–2 μg/ml, and was similar for inhibition of both basal and stimulated release of [3H]phosphatidylcholine. Inhibitory effects of were noted following a 1 h exposure to compound and persisted up to 3 h. The inhibitory effect of compound was entirely reversed by removing compound from the external milieu. Compound had no effect on cytosolic cyclic AMP levels or lactate dehydrogenase release. Inhibition of surfactant release produced by compound was unaffected by changes in extracellular calcium concentrations. Compound is a non-toxic inhibitor of phosphatidylcholine release from Type II epithelial cells. 相似文献
4.
A L Flowers D A Hessinger 《Biochemical and biophysical research communications》1981,103(3):1083-1091
Nematocyst venom from Portuguese Man-of War ( sp.) tentacles causes isolated rat peritoneal mast cells to release histamine. Extent of histamine release is dose-dependent (K0.5 = 6.1 μg venom/ml) and attains 100% at high doses of venom. Release is independent of intra- and extracellular calcium levels and does not depend upon a cellular supply of ATP. The rate of histamine release is temperature-dependent and the extent of release is maximized broadly over the range of 10–30°C. The cytoplasmic marker lactate dehydrogenase, is released concomitantly with histamine but is more sensitive to the venom (K0.5 = 2.1 μg/ml). Antimycin A, while it does not significantly affect venom-induced histamine release, increases the sensitivity of lactate dehydrogenase release (K0.5 = 0.2 μg/ml). We conclude that nematocyst venom induces the release of histamine from mast cells by a cytolytic mechanism and that this action is antagonized by an intracellular, energy-requiring process. 相似文献
5.
The adenosine triphosphate (ATP) content of rat mast cells was studied during and after histamine release induced by compound 48/80. The almost identical time course of ATP decrease from mast cells treated with either glycolytic or respiratory inhibitors seems to indicate that the ATP depletion was largely related to the histamine release process and not to an uncoupling of the oxidative phosphorylation. These results support the view that histamine release induced by compound 48/80 is an energy-requiring process. The ATP content of the cells was not, however, restored within the two hours of observation. The cause of the prolonged decrease in the ATP level has been discussed. 相似文献
6.
Hisashi Shibata Mitsunobu Mio Kenji Tasaka 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1984,805(1):127-130
When compound , a potent histamine liberator, was added in the aqueous phase facing the black lipid membrane, the conductivity of the membrane was remarkably increased. Although valinomycin displayed a distinct selectivity for K+ movement, such selection for ionic permeability was not observed in the case of compound . 相似文献
7.
Exposure of rat peritoneal mast cells to magnesium in the absence of extracellular calcium resulted in a time- and dose-dependent decrease in the secretory response induced by compound 48/80. The decrease was prevented by a low extracellular concentration of calcium. Furthermore, the decreased secretory responsiveness was dose-dependently restored by the addition of calcium to the cells simultaneously with compound 48/80. Preincubation with magnesium also inhibited antigen-induced histamine secretion in a dose-dependent manner. This was reversed by the simultaneous addition of calcium and the secretory stimulus. A dose-dependent decrease in antigen induced histamine secretion that was reversed by calcium was also observed. Exposure of the mast cells to magnesium for 15 min resulted in a parallel decrease in histamine secretion and in the cellular content of 45Ca2+. These observations suggest that magnesium may decrease the secretory response by displacing the cellular calcium which is utilized in stimulus-secretion coupling. 相似文献
8.
Keith Barrett-Bee 《Biochemical and biophysical research communications》1981,98(2):397-403
Antigen stimulated release of histamine from sensitized guineapig lung was inhibited by the exclusion of calcium ions from the incubation fluid. Subsequent addition of calcium ions induced release, but the magnitude of this release decreased with time. When the releasing potential had declined to zero, addition of an alternative antigen together with calcium ions induced further release. If the primary challenge was inhibited by the presence of an antiallergic agent, challenge by a second antigen was similarly inhibited, in contrast to the effect when there was no primary antigen challenge. Antigen challenge induced a flux of into cells, these fluxes were inhibited by compounds which inhibited histamine release. Inhibition of release did not correlate with inhibition of calcium flux with some agents, suggesting that the measured flux is the sum of at least two fluxes, one secondary to release. These results are explained in a scheme for antigen-induced histamine release. 相似文献
9.
Choi IY Moon PD Koo HN Myung NY Kim SJ Lee JH Han SH Moon G Seo SY Sung HJ Park RK Jeong HJ Um JY Kim HM Hong SH 《In vitro cellular & developmental biology. Animal》2007,43(7):215-221
To explore effects of Forsythia koreana methanol extract (FKME) on mast cell-mediated allergic and inflammatory properties, the effect of FKME was evaluated on compound
48/80-induced systemic anaphylaxis, ear swelling, and anti-dinitrophenyl (DNP) immunoglobulin E (IgE)-induced passive cutaneous
anaphylaxis (PCA). In addition, the effect of FKME was investigated on the histamine release from rat peritoneal mast cells
(RPMCs) stimulated by compound 48/80, which promotes histamine release. The human mast cell line HMC-1 was stimulated by phorbol
12-myristate 13-acetate plus calcium ionophore A23187. Activated HMC-1 can produce several proinflammatory and chemotactic
cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-8. Cytokine levels in the culture supernatant
were measured by an enzyme-linked immunosorbent assay. Cytotoxicity by FKME was determined by a 3-(4,5-dimethylthiazol-2-yl)-diphenyl-tetrazolium
bromide (MTT) assay. FKME inhibited compound 48/80-induced systemic anaphylactic shock and ear swelling in mice. When 1 g/kg
FKME was pretreated or posttreated with mice, compound 48/80-induced mice morality was 50 and 66.7%, respectively. One gram
per kilogram of FKME pretreatment inhibited ear-swelling responses derived from compound 48/80 by 29.75%. A PCA reaction was
inhibited by 17.9%. In an in vitro model, FKME (1 mg/ml) inhibited histamine release from the RPMCs by 13.8% and TNF-α, IL-6,
and IL-8 production from HMC-1 cells by 71.16% (P < 0.001), 86.72% (P < 0.001), and 44.6%, respectively. However, FKME had no cytotoxic effects on cell viability. In conclusion, FKME inhibited
not only systemic anaphylaxis and ear swelling induced by compound 48/80 but also inhibited a PCA reaction induced by anti-DNP
IgE in vivo. Treatment with FKME showed significant inhibitory effects on histamine, TNF-α, IL-6, and IL-8 release from mast
cells. 相似文献
10.
The possible role of calcium in the uptake of transferrin and iron by rabbit reticulocytes was investigated by altering cellular calcium levels through the use of the chelating agents EDTA and acid (EGTA) and the ionophores, A23187 and X537A. Incubation of reticuloyctes with EDTA or EGTA at 4°C had no effect on transferrin and iron uptake but incubation at 37°C resulted in an irreversible inhibition associated with decreased adsorption of transferrin to the cells and evidence of inactivation or loss of the transferrin receptors. Transferrin and iron uptake were also inhibited when the cells were incubated with A23187 or X537A. In the case of A23187 the action was primarily exerted on the temperature-sensitive stage of transferrin uptake and was associated with loss of cellular K+ and decrease in cell size. The effect was greater when Ca2+ was added to the incubation medium than its absence. X537A produced relatively greater inhibition of iron uptake than of transferrin uptake, associated with a reduction in cellular ATP concentratio. The action of X537A was unaffected by the presence of Ca2+ in the incubation medium.The results obtained with EDTA and EGTA indicate that cell membrane Ca2+ is required for the integrity or binding of transferrin receptors to the reticulocyte membrane. No evidence was obtained from the experiments with ionophores that an increase of cellular Ca2+ affects transferrin and iron uptake directly. The inhibition caused by A23187 was mainly due to a reduction in cell size resulting from increased membrane permeability to K+ and that caused by X537A appeared to result from an inhibition of energy metabolism and ATP production. 相似文献
11.
In this study, we investigated the effect of Amomum xanthiodes (Zingiberaceae) extract (AXE) on the mast cell-mediated allergy model and studied the possible mechanism of action. We found that AXE inhibited compound 48/80-induced systemic reactions and plasma histamine release in mice. Additionally, AXE decreased immunoglobulin E (IgE)-mediated local allergic reactions and passive cutaneous anaphylaxis (PCA), and AXE dose-dependently attenuated the release of histamine from rat peritoneal mast cells (RPMC) activated by compound 48/80 or IgE. The amounts of AXE needed for inhibition of compound 48/80-induced plasma histamine release and PCA were similar to disodium cromoglycate, the known anti-allergic drug. We found that AXE increased the cAMP levels and decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AXE attenuated the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187)-stimulated tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 secretion in human mast cells. The inhibitory effect of AXE on the proinflammatory cytokines was nuclear factor-kappaB (NF-kappaB)-dependent. In addition, AXE decreased PMA plus A23187-induced degradation of IkappaBalphaand the nuclear translocation of NF-kappaB. Our findings provide evidence that AXE inhibits mast cell-derived immediate-type allergic reactions, and that cAMP, intracellular Ca2+, proinflammatory cytokines, and NF-kappaB are involved in these effects. 相似文献
12.
I S Gushchin M E Kaminka I L Deriugin 《Biulleten' eksperimental'no? biologii i meditsiny》1978,86(10):471-474
Phenothiazines (chlorpromazine and promethazine) and antihistaminic quinuclidine derivatives [phencarol, quinuclidyl-3-di-(o-tolyl) carbinol, hydrochloride quinuclidyl-3-di-(o-methoxyphenyl) carbinol--HQMC] at concentrations preceding the histamine-releasing ones inhibited the compound 48/80-induced histamine release from the isolated rat mast cells. HQMC inhibited histamine release induced by selective liberators (compound 48/80, MCD-peptide, specific antigen), but potentiated histamine release induced by nonselective liberators (chlorpromazine, tryton X-100). The inhibition by HQMC of histamine release induced by compound 48/80 increased during 1 min and was reversible. The inhibitory effect of all the compounds tested was partially counteracted by glucose. 相似文献
13.
Klaus Gietzen Peter Adamczyk-Engelmann Andreas Wüthrich Anka Konstantinova Hermann Bader 《生物化学与生物物理学报:生物膜》1983,736(1):109-118
Compound , a condensation product of N-methyl-p-methoxyphenethylamine with formaldehyde, is composed of a family of cationic amphiphiles differing in the degree of polymerization. Compound was found to be a potent inhibitor of the calmodulin-activated fraction of brain phosphodiesterase and red blood cell Ca2+-transport ATPase, with IC50 values of 0.3 and 0.85 μg/ml, respectively. However, the basal activity of both enzymes is not at all suppressed by the drug at concentrations up to 300 μg/ml. Inhibition of Ca2+ transport into inside-out red blood cell vesicles by compound follows a similar pattern in that basal, calmodulin-independent, transport is also not affected by the drug. Kinetic analysis revealed that the stimulation of Ca2+-transport ATPase induced by calmodulin is inhibited by compound according to a competitive mechanism. It was demonstrated that the inhibitory constituents of compound bind to calmodulin in a Ca2+-dependent fashion. Comparison of the specificity of several anti-calmodulin drugs showed that compound is the most specific inhibitor of the calmodulin-dependent fraction of red blood cell Ca2+-transport ATPase that has been described hitherto. In addition, compound was found to be a rather specific inhibitor of the calmodulin-induced activation of Ca2+-transport ATPase when compared with the stimulation induced by an anionic amphiphile or by limited proteolysis. Half-maximal inhibition of the activity stimulated by oleic acid or mild tryptic digestion required 8- and 32-times higher concentrations of compound , respectively, compared with the calmodulin-dependent fraction of the ATPase activity. Moreover, calmodulin-independent systems as rabbit skeletal muscle sarcoplasmic reticulum Ca2+-transport ATPase or calf cardiac sarcolemma (Na+ + K+)-transport ATPase are far less influenced by compound as compared with trifluoperazine and calmidazolium. Because of its high specificity compound is proposed to be a promising tool for studying calmodulin-dependent processes. 相似文献
14.
The crosstalk between 3', 5'-cyclic adenosine monophosphate (cAMP), intracellular calcium, and histamine release in rat mast cells using the stimulatory effect of three different drugs, thapsigargin, sodium fluoride (NaF), and compound 48/80 were studied. Each of these drugs induces histamine release by different mechanisms. The transducting pathways modulating cAMP and intracellular calcium levels were modified by using, cholera toxin (CTX) which ADP-rybosylates Gs-protein, pertussis toxin (PTX) which ADP-rybosylates Gi-protein, and okadaic acid (OA) which inhibits phosphatases 1 and 2a. Our results show that CTX increased cAMP levels and inhibited histamine release elicited by thapsigargin and compound 48/80. The inhibitory effect of CTX on histamine release was potentiated by OA in the presence of compound 48/80 but was decreased in the presence of thapsigargin. Calcium uptake was stimulated by NaF and compound 48/80. The previous treatment with OA increased calcium uptake when combined with compound 48/80 but not with NaF. Treatment with NaF highly stimulated calcium uptake and cAMP levels only when combined with OA and CTX. These results suggest that the modulatory effect of intracellular calcium and cAMP on histamine release depend more on the crosstalk of the activated signal transducting pathway than on the final level of calcium or cAMP, further supporting the theory that rat mast cells are divided into functionally distinct compartments. 相似文献
15.
Cyclic 3',5'-AMP phosphodiesterase of Neurospora crassa 总被引:13,自引:0,他引:13
Cyclic 3′,5′-AMP (cAMP) phosphodiesterase activity can be demonstrated in extracts of . The activity is particulate, has a pH optimum of 7.4, and consists of two forms that have different cAMP binding constants. Methylxanthines, inorganic phosphate, and EDTA are inhibitors of the diesterase as are ATP, ADP, and 8-bromo-cAMP. The enzymatic activity is stimulated by histamine and imidazole. These properties suggest that the enzyme is more closely related to the mammalian than to bacterial cAMP phosphodiesterases. 相似文献
16.
F F Campo M Hernández-Asensio J M Ramírez 《Biochemical and biophysical research communications》1975,63(4):1099-1105
The initial rate of uptake of methyl α-D-glucopyranoside by is inhibited by respiration. The inhibition is more pronounced in mutant strains which cannot use the energy-rich state of the membrane to form ATP because of a defective Ca2+, Mg2+-activated ATPase. In both mutant and normal strains, the inhibition of glucoside uptake is not accompanied by an increase of the ATP content of the cells and is abolished by carbonyl cyanide -chlorophenylhydrazone, a drug which dissipates membrane energy. It appears, therefore, that the inhibitory effect of respiration is mediated by the energy-rich state of the membrane and that ATP does not participate in the inhibition. 相似文献
17.
The effects of tannins and related polyphenols on KO2- and compound 48/80-induced histamine release from rat peritoneal mast cells were examined. Pretreatment with hydrolyzable tannins (1-100 microM) significantly inhibited KO2-induced histamine release. Dimeric ellagitannins, which have hexahydroxydiphenoyl (HHDP) and valoneoyl residues and/or a valoneoyl-related acyl unit in the molecule, showed more potent inhibitory effects than monomeric hydrolyzable tannins. The most effective inhibition was exhibited by agrimoniin and euphorbin C (IC50 0.68 and 0.80 microM), which have dehydrodigalloyl and euphorbinoyl groups, respectively, as well as the HHDP group. However, procyanidins, flavonoids and related polyphenols with small molecular weights, except for epigallocatechin gallate, exhibited negligible effects. Although clinically used antiallergic drugs, azelastine, astemizole, ketotifen and epinastine have been shown to prevent KO2-induced histamine release, their potencies were all less than those of ellagitannins. An inhibitory effect on compound 48/80-induced histamine release was also exhibited by higher molecular weight tannins. The inhibitory effect on histamine release caused by different stimulants suggested that ellagitannins act as cell membrane stabilizers as well as radical scavengers. 相似文献
18.
D D Hackney 《Biochemical and biophysical research communications》1979,91(1):233-238
The soluble mitochondrial ATPase, F1, can be slowly inactivated by incubation with Mg+2 in a manner consistent with the observations of Moyle and Mitchell , 55 (1975)). This inhibition results in a low initial rate of ATP hydrolysis upon addition to an ATPase assay medium of F1 which has been incubated with Mg+2. This inhibition, however, is completely reversible by Mg·ATP in a time dependent process and results in the rate of ATP hydrolysis increasing during the ATPase assay to reach control levels after 30 sec. The length of the lag is independent of the F1 concentration in the ATPase assay and the lag is also completely reversed by subsequent incubation with excess EDTA before assay.F1 is unstable if incubated with EDTA in the absence of free nucleotides or Mg+2. The rate of inactivation increases with decreasing protein concentration until a limiting rate is reached at high dilution. Mg+2 in excess of the EDTA or 50 μM ADP stabilize the F1 against the inactivation but cannot reverse prior denaturation. 相似文献
19.
20.
When retinol was incubated in the presence of ATP, UDP-galactose, magnesium ions and Triton X-100, with a whole homogenate of rat thyroid as an enzyme source the formation of a retinol containing phosphate compound was observed besides retinol galactoside described before. This phosphate compound is soluble in chloroform-methanol (3:2, ) and can be separated by chromatography on a column prepared with butanol-washed cellulose powder. The isolated compound was retinol pyrophosphate since it contained retinol and phosphate in a molar ratio of 1:2 shown by double isotopic labelling techniques and was found to be free of galactose. 相似文献