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Joanna Bonior, Jolanta Jaworek, Anna Leja-Szpak, Michalina Kot, Magdalena Macko, Romana Tomaszewska, Jerzy Stachura, Stanisław J Konturek, Wiesław W Pawlik
Med Sci Tech 2005; 46(3): RA39-46
ID: 881463
Background: Ghrelin, a peptide originally isolated from the stomach, has been also identifiedinthebrain.Ghrelin protects the gastric mucosa from acute damage, stimulates growth hormone (GH) release and affects pancreaticexocrine and endocrine secretions. Ghrelin receptors has been detected in the pancreas but the role of ghrelin in the pancreatic protection is unclear. Aim of the study: To determine the effects of peripheral application of ghrelinon the course of caerulein-induced pancreatitis (CIP) and to investigate the involvement of sensory nerves (SN) in above effects. Methods: The study was carried out on the Wistarrats with intact SN or capsaicin-deactivated SN. To deactivate SN capsaicin was given to one group of rats at total dose of 100 mg/kg 10 days before the tests. CIP was induced by subcutaneous (s.c.) caerulein infusion (25 μg/kg) to the conscious rats. Ghrelin was given to the rats intraperitoneally (i.p.) at doses of 10, 20, 40 or 50 μg/kg 30 min prior to the start of CIP. Plasma level of ghrelin was measured by radioimmunoessey (RIA). Results: CIP was confirmed by histological assessment and characterized by usualedema and rise of plasma lipase activity. Peripheral application of increasing concentration of ghrelin (i. p.) resulted in the dose-dependent rise of plasma level of ghrelin. Ghrelin given i.p. at doses of 20, 40 or 50 μg/kg, 30 min prior to the start of CIP prevented from the acute pancreatitis. These effects were reversed in the rats with capsaicin-deactivated SN.Conclusions: Ghrelin prevents from the development of acute pancreatitis though activation of central mechanisms. (Clin. Exp. Med. Lett. 2005; 46(3):39-46)
Keywords: acute pancreatitis, plasma ghrelin activity