Anti-inflammatory effect of acute stress on experimental colitis is mediated by cholecystokinin-B receptors

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Gulpinar M. A., Ozbeyli D., Arbak S., Yegen B.

LIFE SCIENCES, cilt.75, sa.1, ss.77-91, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 75 Sayı: 1
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1016/j.lfs.2003.12.009
  • Dergi Adı: LIFE SCIENCES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.77-91
  • Anahtar Kelimeler: cholecystokinin (CCK), colitis, hypothalamo-pituitary-adrenal (HPA) axis, stress, sympathetic nervous system (SNS), CORTICOTROPIN-RELEASING-FACTOR, GASTROINTESTINAL-TRACT, ARGININE-VASOPRESSIN, GENE-EXPRESSION, SOCIAL STRESS, C-FOS, CRF, RATS, INFLAMMATION, ACTIVATION
  • Marmara Üniversitesi Adresli: Evet

Özet

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 mug/kg) or cholecystokinin (CCKB; 20 mug/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. (C) 2004 Elsevier Inc. All rights reserved.