title: Anti-inflammatory effect of acute stress on experimental colitis is mediated by cholecystokinin-B receptors.
abstract: We aimed to investigate the effects of electric shock (ES) on the course of experimental colitis and the involvement of possible central and peripheral mechanisms. In Sprague-Dawley rats (n = 190) colitis was induced by intracolonic administration 2,4,6-trinitrobenzenesulfonic acid (TNBS). The effects of ES (0.3-0.5 mA) or the central administration of corticotropin-releasing factor (CRF; astressin, 10 microg/kg) or cholecystokinin (CCKB; 20 microg/kg) receptor antagonists and peripheral glucocorticoid receptor (RU-486; 10 mg/kg) or ganglion (hexamethonium; 15 mg/kg) blockers on TNBS-induced colitis were studied by the assessment of macroscopic score, histological analysis and tissue myeloperoxidase activity. ES reduced all colonic damage scores (p < 0.05-0.01), while central CRF (p < 0.05-0.001) and CCKB receptor (p < 0.05-0.01) blockers or peripheral hexamethonium (p < 0.05-0.01) and RU-486 (p < 0.05) reversed stress-induced improvement. ES demonstrated an anti-inflammatory effect on colitis, which appears to be mediated by central CRF and CCK receptors with the participation of hypothalamo-pituitary-adrenal axis and the sympathetic nervous system.
authors.affiliation: Department of Physiology, Marmara University School of Medicine, Haydarpaşa, 81326 Istanbul, Turkey.
authors.forename: Mehmet Ali
authors.initials: MA
authors.lastname: Gülpinar
authors.forename: Dilek
authors.initials: D
authors.lastname: Ozbeyli
authors.forename: Serap
authors.initials: S
authors.lastname: Arbak
authors.forename: Berrak C
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000208:Acute Disease; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000473:pathology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005730:Ganglionic Blockers / Q000008:administration & dosage / Q000494:pharmacology; D018738:Hexamethonium / Q000008:administration & dosage / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000502:physiology; D007276:Injections, Intraventricular; D007413:Intestinal Mucosa / Q000187:drug effects / Q000473:pathology; D008297:Male; D015735:Mifepristone / Q000008:administration & dosage / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000008:administration & dosage / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043887:Receptor, Cholecystokinin B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000378:metabolism* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000502:physiology; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity
chemical_list: D005730:Ganglionic Blockers; D018377:Neurotransmitter Agents; D043887:Receptor, Cholecystokinin B; D015735:Mifepristone; D018738:Hexamethonium; D014302:Trinitrobenzenesulfonic Acid