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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 2834386, 7 pages
Research Article

Obestatin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

1Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street, 31-531 Cracow, Poland
2Department of Anatomy, Jagiellonian University Medical College, 12 Kopernika Street, 31-034 Cracow, Poland
3Department of Medical Physiology, Faculty of Health Sciences, Jagiellonian University Medical College, 12 Michałowskiego Street, 31-126 Cracow, Poland
4Chair of Clinical Biochemistry, Department of Diagnostics, Jagiellonian University Medical College, 15a Kopernika Street, 31-501 Cracow, Poland
5Department of Internal Medicine II, Thuringia Clinic, Teaching Hospital of the University of Jena, Rainweg 68, 07318 Saalfeld, Germany
6Faculty of Physical Education and Sport, University of Physical Education, 78 Jan Paweł II Street, 31-571 Cracow, Poland

Received 14 July 2015; Revised 29 September 2015; Accepted 12 October 2015

Academic Editor: Tanea T. Reed

Copyright © 2016 Aleksandra Matuszyk et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Obestatin, a 23-amino acid peptide derived from the proghrelin, has been shown to exhibit some protective and therapeutic effects in the gut. The aim of present study was to determine the effect of obestatin administration on the course of acetic acid-induced colitis in rats. Materials and Methods. Studies have been performed on male Wistar rats. Colitis was induced by a rectal enema with 3.5% acetic acid solution. Obestatin was administered intraperitoneally twice a day at a dose of 8 nmol/kg, starting 24 h after the induction of colitis. Seven or 14 days after the induction of colitis, the healing rate of the colon was evaluated. Results. Treatment with obestatin after induction of colitis accelerated the healing of colonic wall damage and this effect was associated with a decrease in the colitis-evoked increase in mucosal activity of myeloperoxidase and content of interleukin-1β. Moreover, obestatin administration significantly reversed the colitis-evoked decrease in mucosal blood flow and DNA synthesis. Conclusion. Administration of exogenous obestatin exhibits therapeutic effects in the course of acetic acid-induced colitis and this effect is related, at least in part, to the obestatin-evoked anti-inflammatory effect, an improvement of local blood flow, and an increase in cell proliferation in colonic mucosa.