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Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats
Fatma A Gultekin1, Ali U Emre1, Sevim K Celik2, Figen Barut3, Ufuk Tali4, Demet Sumer5, Ummuhani O Turkcu6
1 Department of General Surgery, School of Medicine, Bulent Ecevit University, Zonguldak, Turkey
2 Department of Medical Biology, School of Medicine, Bulent Ecevit University, Zonguldak, Turkey
3 Department of Pathology, School of Medicine, Bulent Ecevit University, Zonguldak, Turkey
4 Department of General Surgery, Can Goverment Hospital, Çanakkale, Turkey
5 Department of General Surgery, Nevsehir Goverment Hospital, Nevsehir, Turkey
6 Department of Medical Biochemistry, Mugla School of Health Sciences, Mugla Sitki Kocman University, Mugla, Turkey
Correspondence Address:
Fatma A Gultekin
Department of General Surgery, School of Medicine, Bulent Ecevit University, Zonguldak - 67600
Turkey
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/sjg.SJG_318_16
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Background/Aim: The excessive apoptosis of intestinal epithelial cells (IECs) partly accounts for the development of colonic inflammation and eventually results in ulcerative colitis (UC). Humanin, an endogenous anti-apoptotic peptide, has previously been shown to protect against Alzheimer's disease and a variety of cellular insults. The present study aimed to investigate the effects of glysin variant of humanin (HNG) on 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Materials and Methods: Rats were divided into four groups as follows: Group 1 (n = 8): control; isotonic saline solution 0.1 ml/rat rectally, Group 2 (n = 8): TNBS colitis; 0.1 ml of a 2.5% (w/v) TNBS solution in 50% ethanol rectally, Group 3 (n = 8): 10 μM HNG, and Group 4 (n = 8): 20 μM HNG intraperitoneal (ip) on day 2 and 6 after rectal TNBS administration. Rats were sacrificed 7 days after the induction of colitis. Blood and tissue samples were harvested for biochemical and histopathological analysis. Results: HNG treatment significantly ameliorated weight loss and macroscopic and microscopic scores. TNBS-induced colitis significantly increased the colonic mRNA expression of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and caspase-3 activities in group II in comparison to the group I. HNG treatment was associated with an inhibition of mRNA expression of TNF-α and IL-1β, and a decrease in caspase-3 activities in colon tissues in group III and IV when compared to group II. Conclusion: The results of this study indicate that HNG treatment may exert beneficial effects in UC by decreasing inflammatory reactions and apoptosis. |
