Favourable effects of whey protein upon acetic acid-induced ulcerative colitis in rat model

Author:

TUNC Nurettin1ORCID,SAHİN abdurahman2,DEMİREL Ulvi2,ARTAS Gokhan3,SAHİN Kazım4,BAHCECİOGLU İbrahim2,YALNİZ Mehmet2

Affiliation:

1. Department of Gasttroenterology, Health Sciences University Gazi Yasargil Training and Research Hospital, 21070, Diyarbakir, Turkey

2. Department of Gastroenterology, School of Medicine, Firat University, 23200 Elazig, Turkey

3. Department of Pathology, School of Medicine, Firat University, Elazig, Turkey

4. Department of Animal Nutrition, Faculty of Veterinary Science, Firat University, Elazig, Turkey

Abstract

IntroductionIn the context of the present study, we have aimed to examine the effects of the administration of whey protein through rectal enema to a acetic acid-induced ulcerative colitis in rats on the pathways of nuclear-related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), nuclear factor kappa B (NF-κB), active protein kinase-1 (AP-1), tumour necrotising factor-alpha (TNF-α), and cyclooxygenase-2 (COX-2), IL-6, IL-10.Material and methods28 rats were employed for the trial. Ulcerative colitis was induced through the use of acetic acid. The therapeutic doses of whey protein were administered rectally. Ulcerative colitis was made subject to histopathological examination and protein levels in colon tissue measured with the Western Blot Method.ResultsThe significant increases observed in the levels of AP-1, COX-2, IL-6, IL-10, NF-κβ, and TNF-α as markers of inflammation following the development of ulcerative colitis enjoyed remarkable decreases along with the administration of whey protein (p<0.05). On the other hand, we identified a decrease in the Nrf2-ARE signal pathway and HO-1 protein assuming protective roles on the colon inflammatory response along with the development of ulcerative colitis and an activation of the Nrf2-HO-1 pathway by the whey protein.ConclusionsWhey protein modulates Nrf2/HO-1 and NF-kB pathways, thereby creating a therapeutic effect against colonic inflammation induced by acetic acid (AA) by reason of its anti-inflammatory implications.

Publisher

Termedia Sp. z.o.o.

Subject

General Medicine

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