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Exogenous Ghrelin Accelerates the Healing of Acetic Acid-Induced Colitis in Rats

Previous studies have shown that ghrelin reduces colonic inflammation induced by trinitrobenzene sulfonic acid and dextran sodium sulfate. In the present study we determined the effect of treatment with ghrelin on the course of acetic acid-induced colitis in rats. Rectal administration of 3% acetic...

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Published in:International journal of molecular sciences 2016-09, Vol.17 (9), p.1455-1455
Main Authors: Matuszyk, Aleksandra, Ceranowicz, Piotr, Warzecha, Zygmunt, Cieszkowski, Jakub, Ceranowicz, Dagmara, Gałązka, Krystyna, Bonior, Joanna, Jaworek, Jolanta, Bartuś, Krzysztof, Gil, Krzysztof, Olszanecki, Rafał, Dembiński, Artur
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Language:English
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Summary:Previous studies have shown that ghrelin reduces colonic inflammation induced by trinitrobenzene sulfonic acid and dextran sodium sulfate. In the present study we determined the effect of treatment with ghrelin on the course of acetic acid-induced colitis in rats. Rectal administration of 3% acetic acid solution led to induction of colitis in all animals. Damage of the colonic wall was accompanied by an increase in mucosal concentration of pro-inflammatory interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), as well mucosal activity of myeloperoxidase. Moreover, induction of colitis led to a reduction in colonic blood flow and DNA synthesis. Administration of ghrelin after induction of colitis led to faster regeneration of the colonic wall and reduction in colonic levels of IL-1β, TNF-α, and myeloperoxidase. In addition, treatment with ghrelin improved mucosal DNA synthesis and blood flow. Our study disclosed that ghrelin exhibits a strong anti-inflammatory and healing effect in acetic acid-induced colitis. Our current observation in association with previous findings that ghrelin exhibits curative effect in trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis suggest that therapeutic effect of ghrelin in the colon is universal and independent of the primary cause of colitis.
ISSN:1422-0067
1422-0067
DOI:10.3390/ijms17091455