1,721,099 research outputs found
Hydrocortisone and 'macrocortin' inhibit the zymosan-induced release of lyso-PAF from rat peritoneal leucocytes.
No full textHydrocortisone and the glucocorticoid-induced anti-phospholipase protein macrocortin, were tested as inhibitors of PAF generation. The steroid produced a dose-dependent inhibition of the release of the PAF precursor 2-lyso-PAF, and this effect was mimicked by affinity-purified macrocortin. Neither agent had any effect on the acetylation of lyso-PAF to PAF. Of other drugs tested only phospholipase inhibitors blocked lyso-PAF release and sulphydryl reagents blocked the acetylation step. It is concluded that glucocorticoids inhibit the generation of PAF and this could be an important component of their anti-anaphylactic and anti-inflammatory action
Human recombinant lipocortin 1 inhibits prostacyclin production by human umbilical artery in vitro.
No full textSubmicromolar concentrations of human recombinant Lipocortin 1 inhibit the release of prostacyclin from human umbilical artery rings in a dose-dependent fashion. This is the first demonstration that the recombinant protein is effective in human cells
Peptide 204-212 of lipocortin 5 inhibits the generation of a prostacyclin-like factor from rat aorta preparations in vitro.
No full textA comparison of the acute inflammatory response in adrenalectomised and sham-operated rats.
No full textCarrageenin pleurisy was induced in adrenalectomised (ADX) and sham-operated (SHO) rats. The magnitude and duration of inflammation, as estimated by fluid exudation and cell migration, was greatly increased (approximately doubled) in ADX rats compared with that in their SHO controls. The content of eicosanoids (6-keto-prostaglandin F1 alpha (6-keto-PGF 1 alpha), thromboxane B2 (TXB2), and leukotriene B4 (LTB4] in inflammatory exudates from ADX rats was significantly (2-4 fold) greater than that of their SHO controls. Resident macrophages obtained from ADX rats produced more eicosanoids per cell per unit time when stimulated in vitro with zymosan, than did cells from the SHO controls. Administration of glucocorticoids blocked the inflammatory response and reduced the release of eicosanoids both in vitro and in vivo in both groups of rats. These data are consistent with the notion that physiological amounts of glucocorticoids exert a tonic inhibitory action on phospholipase activity in normal animals and that the increased secretion of these hormones during the inflammatory response serves to check and control the development of inflammation
The inhibition by hydrocortisone of prostaglandin biosynthesis in rat peritoneal leucocytes is correlated with intracellular macrocortin levels
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Human recombinant lipocortin 1 has acute local anti-inflammatory properties in the rat paw edema test.
No full textHuman recombinant lipocortin 1 has been tested for anti-inflammatory activity in a conventional model of acute inflammation. Microgram amounts of the protein, locally administered, inhibited edema of the rat paw when induced by subplantar injections of carrageenin: the ED50 was 10-20 micrograms per paw, and inhibition (maximum of 60-70\%) was not dependent upon an intact adrenal cortex. Doses of lipocortin that produced approximately 50\% inhibition in the carrageenin test were inactive against edema elicited by bradykinin, serotonin, platelet-activating factor-acether, or dextran, whereas edema caused by Naja mocambique venom phospholipase A2 was strongly inhibited by lipocortin. The protein inhibited edema when rats were pretreated with agents that depleted mast-cell amines, kininogen, or polymorphonuclear leukocytes prior to initiation of the carrageenin edema but had no inhibitory action when rats were pretreated with the dual cyclooxygenase/lipoxygenase inhibitor BW 755C. These results demonstrate that human recombinant lipocortin has potent local anti-inflammatory activity, probably through selectively interfering with eicosanoid generation. Lipocortin is relatively ineffective against edema caused by mast-cell degranulation or kinins, except when degranulation is caused by phospholipase A2
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