الفهرس 
Effect of vildagliptin in treatment of experimentally induced {u2013}ulcerative
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Abstract
Ulcerative colitis (UC) is a chronic bowel disease depicted by the involvement of pro-inflammatory cytokines.The release of these cytokines is regulated by phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor-kappa B (NFmB) and cAMP response element-binding protein (CREB) signaling pathways as well as over expression of microRNA 146a (miR-146a) and long non-coding RNA interferon gamma antisense 1 (lncRNA IFNG-AS1). Vildagliptin (Vilda), a dipeptidyl peptidase IV (DPP-IV) inhibitor, has an anti-inflammatory, antioxidant and anti-apoptotic effects which were established in various models. However, its possible protective effect in UC has not been clarified. Hence, the current study aimed to explore the possible prophylactic effect of different doses of Vilda against acetic acid (AA)-induced UC in rats. Forty-eight adult male Wistar rats were divided into six groups: control, Vilda (10 mg/kg/day; p.o.), AA, AA+Vilda (5 mg/kg/day; p.o.), AA+Vilda (10 mg/kg/day; p.o.) and AA+sulfasalazine (Sulfa) (100 mg/kg/day; p.o.).Low- and high-dose Vilda showed a significant improvement in the disease activity index (DAI) and macroscopic assessment markers. Vilda has markedly modulated the expression of lncRNA IFNG-AS1 and miR-146a, as well as PI3K/Akt/NFmB, CREB and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, which was reflected in alleviated oxidative stress, inflammation and apoptosis. Such outcomes were more prominent with the high-dose Vilda against low-dose Vilda and Sulfa. Moreover, the histological examination showed almost intact histological features in Vilda-treated groups when compared to AA group. In conclusion, Vilda can be regarded as a new promising therapeutic alternative against UC with higher benefit shown with high-dose Vilda