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CAPE Improves Vanin-1/AKT/miRNA-203 Signaling Pathways in DSS-induced Ulcerative Colitis

Azza M. Metwaly 1
Heba M. Elmoghazy 2
Mohammed Abdalla Hussein 2, * ORCID logo
Amal Abdel-Aziz 1
Samir A Elmasry 1
  1. Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), Sadat University, Egypt
  2. Biochemistry Department, Faculty of Applied Medical Sciences, October 6 University, Egypt
Correspondence to: Mohammed Abdalla Hussein, Biochemistry Department, Faculty of Applied Medical Sciences, October 6 University, Egypt. ORCID: https://orcid.org/0000-0002-1811-2794. Email: [email protected].
Volume & Issue: Vol. 9 No. 9 (2022) | Page No.: 5313-5325 | DOI: 10.15419/bmrat.v9i9.769
Published: 2022-09-30

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This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. 

Abstract

Introduction: Ulcerative colitis (UC) and other inflammatory bowel diseases (IBDs) are common chronic, inflammatory gastrointestinal diseases. Due to their antioxidant, anti-inflammatory, and antibacterial properties, polyphenols are beneficial in the treatment of IBD. Caffeine acid phenethyl ester (CAPE) has been shown to have cytotoxic, antibacterial, antioxidant, and anti-inflammatory effects. This study focuses on the biochemical and molecular levels of the mode of action of CAPE in DSS-induced UC in rats.

Methods: Thirty male Wistar rats were distributed into five groups, with six rats in each group: group I was administered 3 mL of distilled water orally, group II was administered CAPE (10 mg/kg.b.w.) orally, group III was administered 5% DSS orally, group IV was administered 5% DSS and CAPE (10 mg/kg.b.w.) orally; and group V was administered 5% DSS and sulfasalazine (100 mg/kg b.w.) orally.

Results: Individually, oral treatment with CAPE or sulfasalazine significantly ameliorated body weight, DAI score, and colon length in DSS-induced colitis and raised blood PLT count, NO, NF-kß, and vitamin C levels. In addition, animals given CAPE had a considerable increase in colon GSH, GPx, CAT, and SOD levels compared with rats given DSS. Compared with the DSS control group, colon TBAR, IL-6, and INF-ɣ were lower in the CAPE-treated rats. Histopathological examination revealed that CAPE treatment caused tissue injury and improved vanin-1, AKT, and miRNA-203 genes in the distal colon and triggered apoptosis.

Conclusions: The gastroprotective impact of CAPE was more noticeable than sulfasalazine. CAPE treatment caused biochemical and histopathological improvements, indicating that CAPE may have antioxidant and anti-inflammatory effects in colitis; therefore, CAPE may be a potential therapeutic agent for the amelioration of IBD. This finding is promising for future therapies and research goals.

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