title: The involvement of glucocorticoids and interleukin-1 in the regulation of brain prostaglandin production in response to surgical stress.
abstract: BACKGROUND
  This study examined the role of glucocorticoids (GC) and interleukin-1 (IL-1) in regulating the production of brain prostaglandin E(2) (PGE(2)) in response to surgical stress.
  
  
  METHODS
  Surgical stress was induced in rats by laparotomy or exploration of the carotid. PGE(2) 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 PGE(2) response to surgical stress was examined in IL-1 receptor type I deficient (IL-1rKO) mice.
  
  
  RESULTS
  Surgical stress elevated serum corticosterone and increased PGE(2) production by the frontal cortex and the central amygdala. A more pronounced PGE(2) response was found in adrenalectomized rats and in rats treated with RU38486, whereas administration of dexamethasone inhibited stress-induced PGE(2) production. IL-1rKO mice exhibited lower PGE(2) production in the frontal cortex under basal condition and failed to increase PGE(2) production in response to surgical stress.
  
  
  CONCLUSIONS
  Surgical stress-induced production of brain PGE(2) is specifically regulated by GC via the mediation of type II corticosteroid receptors. Normal IL-1 signaling is required for the production of brain PGE(2) under basal conditions and in response to surgical stress.
authors.affiliation: Department of Anesthesiology, Rabin Medical Center, Golda-Hasharon Campus, Petah Tiqva, Tel-Aviv University, Jerusalem, Israel.
authors.forename: Benzion
authors.initials: B
authors.lastname: Beilin
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Shavit
authors.forename: Freda
authors.initials: F
authors.lastname: Dekeyser
authors.forename: Anna
authors.initials: A
authors.lastname: Itzik
authors.forename: Joseph
authors.initials: J
authors.lastname: Weidenfeld
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D001921:Brain / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D003907:Dexamethasone / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis / Q000276:immunology; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005938:Glucocorticoids / Q000097:blood / Q000276:immunology*; D007375:Interleukin-1 / Q000235:genetics / Q000276:immunology*; D007813:Laparotomy / Q000009:adverse effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D015213:Neuroimmunomodulation / Q000276:immunology; D011183:Postoperative Complications / Q000276:immunology* / Q000503:physiopathology; D011453:Prostaglandins / Q000096:biosynthesis / Q000276:immunology*; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors / Q000378:metabolism; D013312:Stress, Physiological / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D014656:Vascular Surgical Procedures / Q000009:adverse effects
chemical_list: D005938:Glucocorticoids; D007375:Interleukin-1; D011453:Prostaglandins; D011965:Receptors, Glucocorticoid; D003907:Dexamethasone; D015232:Dinoprostone