Systemic anaphylaxis is prevented in alloxan-diabetic rats by a mechanism dependent on glucocorticoids

This study was undertaken to examine whether glucocorticoids could be implicated in the hyporesponsiveness of diabetic rats to systemic anaphylaxis. Rats were actively sensitized with a mixture of Al(OH) 3 plus ovalbumin and challenged i.v. with ovalbumin 14 days later. Diabetes was induced by allox...

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Veröffentlicht in:European journal of pharmacology 2003-07, Vol.472 (3), p.221-227
Hauptverfasser: Carvalho, Vinicius F., Barreto, Emiliano O., Diaz, Bruno L., Serra, Magda F., Azevedo, Viviane, Cordeiro, Renato S.B., Martins, Marco A., e Silva, Patrı&#x0301, cia M.R.
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container_issue 3
container_start_page 221
container_title European journal of pharmacology
container_volume 472
creator Carvalho, Vinicius F.
Barreto, Emiliano O.
Diaz, Bruno L.
Serra, Magda F.
Azevedo, Viviane
Cordeiro, Renato S.B.
Martins, Marco A.
e Silva, Patrı&#x0301
cia M.R.
description This study was undertaken to examine whether glucocorticoids could be implicated in the hyporesponsiveness of diabetic rats to systemic anaphylaxis. Rats were actively sensitized with a mixture of Al(OH) 3 plus ovalbumin and challenged i.v. with ovalbumin 14 days later. Diabetes was induced by alloxan-injected i.v. either before or after sensitization. Elevation of total and specific serum immunoglobulin E (IgE) was abolished in rats turned diabetic and then sensitised, but not in those first sensitised and then turned diabetic. In both conditions, increased serum corticosterone levels occurred in parallel with protection of diabetic animals against fatal shock, intestinal haemorrhage and elevation in plasma histamine levels evoked by antigen challenge. The resistance of diabetic rats to fatal shock was no longer significantly different from that of non-diabetic rats following treatment with the glucocorticoid receptor antagonist RU 486 (mifepristone). These findings indicate that endogenous glucocorticoid plays a pivotal role in the phenomenon of hyporeactivity to systemic anaphylaxis in alloxan-diabetic rats.
doi_str_mv 10.1016/S0014-2999(03)01934-4
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Rats were actively sensitized with a mixture of Al(OH) 3 plus ovalbumin and challenged i.v. with ovalbumin 14 days later. Diabetes was induced by alloxan-injected i.v. either before or after sensitization. Elevation of total and specific serum immunoglobulin E (IgE) was abolished in rats turned diabetic and then sensitised, but not in those first sensitised and then turned diabetic. In both conditions, increased serum corticosterone levels occurred in parallel with protection of diabetic animals against fatal shock, intestinal haemorrhage and elevation in plasma histamine levels evoked by antigen challenge. The resistance of diabetic rats to fatal shock was no longer significantly different from that of non-diabetic rats following treatment with the glucocorticoid receptor antagonist RU 486 (mifepristone). 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subjects Anaphylaxis - blood
Anaphylaxis - prevention & control
Animals
Biological and medical sciences
Diabetes
Diabetes Mellitus, Experimental - blood
Glucocorticoid
Glucocorticoids - blood
Male
Mast cell
Medical sciences
Mifepristone - pharmacology
Rats
Rats, Wistar
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - metabolism
Systemic anaphylaxis
title Systemic anaphylaxis is prevented in alloxan-diabetic rats by a mechanism dependent on glucocorticoids
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