Background: This study examined the role of glucocorticoids (GC) and interleukin-1 (IL-1) in regulating the production of brain prostaglandin E2 (PGE2) in response to surgical stress. Methods: Surgical stress was induced in rats by laparotomy or exploration of the carotid. PGE2 ex vivo production was measured in the frontal cortex or central amygdala of adrenalectomized rats, or of rats treated with either the GC type II receptor blocker (RU38486) or synthetic GC (dexamethasone). IL-1 involvement in mediating PGE2 response to surgical stress was examined in IL-1 receptor type I deficient (IL-1rKO) mice. Results: Surgical stress elevated serum corticosterone and increased PGE2 production by the frontal cortex and the central amygdala. A more pronounced PGE2 response was found in adrenalectomized rats and in rats treated with RU38486, whereas administration of dexamethasone inhibited stress-induced PGE2 production. IL-1rKO mice exhibited lower PGE2 production in the frontal cortex under basal condition and failed to increase PGE2 production in response to surgical stress. Conclusions: Surgical stress-induced production of brain PGE2 is specifically regulated by GC via the mediation of type II corticosteroid receptors. Normal IL-1 signaling is required for the production of brain PGE2 under basal conditions and in response to surgical stress.

Keywords:
Prostaglandins, Glucocorticoids, Interleukin-1, Surgical stress, Adrenalectomy
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© 2006 S. Karger AG, Basel
2006
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