Therapeutic effects of vitamin D on acetic acid-induced colitis in rats

Refik Bademci,Oytun Erbaş,Ali Yücel Kara,Gürkan Yiğittürk,Mümin Alper Erdoğan

doi:10.1590/s0102-865020200040000004

Abstract

Purpose To analyze the effect of calcitriol treatment on acute colitis in an experimental rat model.Methods A total of 24 adult Sprague Dawley albino rats were randomly separated into 3 equal groups: control group (n:8), colitis group (n:8), calcitriol administered group (n:8). A single dose of acetic acid (1 ml of 4% solution) was administered intrarectally to induce colitis. Group 1 was given 1 ml/kg 0.9% NaCl intraperitoneally; rats belonging to Group 2 were administered calcitriol 1 µg/kg for 5 days.Results Plasma tumor necrosis factor alpha, Pentraxin 3, and malondialdehyde levels were significantly lower in the calcitriol administered colitis group than in the standard colitis group (p<0.01). In the Calcitriol group, there was a significant histological improvement in hyperemia, hemorrhage and necrotic areas in the epithelium compared to the placebo group (p <0.000).Conclusion The findings suggest that calcitriol may be an agent that could be used in acute colitis treatment.

Highlights

Inflammatory bowel disease (IBD) is a condition generally typified by idiopathic, repetitive and often diffuse inflammation of the colon and the rectum mucosa
Placebo group and the Vitamin D group were compared in a histopathological manner, the colitis group showed a higher ratio of hyperemia: hemorrhage and necrotic areas in the epithelium (p
Acute colitis conditions require medical agents to stabilize the patients. It has been shown in some experimental colitis studies that vitamin D is useful for healthy bowel operation[22], and that the loss or overexpression of Vitamin D Receptor (VDR) expression, worsens or alleviates symptoms in experimental colitis models, respectively, and it is seen as a potential cause of increased mucosal permeability, increased intestinal epithelial cell apoptosis, increased mucosal bacterial burden, and increased colitis symptoms in autophagy[22,23]

Summary

Introduction

Inflammatory bowel disease (IBD) is a condition generally typified by idiopathic, repetitive and often diffuse inflammation of the colon and the rectum mucosa. Though the etiology of IBD is not yet fully comprehended, many genetic, environmental and immunological factors play a role and it is thought that intestinal microflora, mucosal immunoreaction, autoimmune reactions and especially oxidative stress, play a role in the pathophysiology of IBD1,2. Many inflammatory factors such as TNF-α, malondialdehyde (MDA), and pentraxin-3, increase in levels parallel with an increase in IBD inflammation, and histological evidence of inflammation in tissues can be observed[3]. Excessive inflammation and oxidative stress have pivotal roles in ulcerative colitis disease pathogenesis[3]. Evidence suggests that the cascade of free radical production and subsequent lipid peroxidation reduce the cellular antioxidant capacity, resulting in colonic inflammation

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