Date Published: June 12, 2020
Publisher: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
Author(s): Refik Bademci, Mümin Alper Erdoğan, Ali Yücel Kara, Gürkan Yiğittürk, Oytun Erbaş.
To analyze the effect of calcitriol treatment on acute colitis in an experimental rat model.
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.
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). The findings suggest that calcitriol may be an agent that could be used in acute colitis treatment.
Inflammatory bowel disease (IBD) is a condition generally typified by idiopathic, repetitive and often diffuse inflammation of the colon and the rectum mucosa. Ulcerative colitis (UC) and Crohn’s disease (CD) are the major subtypes of IBD. 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 thus histological evidence of inflammation in tissues can be observed3.
When the control group, 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 <0.01) compared to the placebo group and the vitamin D group (p <0.01). In the group receiving vitamin D, hyperemia, hemorrhage and necrotic areas showed a significant improvement (p <0.000) (Table 1, Fig. 1). The chronic condition of IBD lowers the life quality for the many of the people who have been affected. It usually manifests with destruction of the colon mucosa and consequent diarrhea attacks. Surgical treatments may be curative, as extensive resections reduce the life quality and medical treatments are generally preferred for cases with limited, mild and moderate inflammation16. Acute colitis hemorrhage is a condition of high mortality and morbidity for surgeons, which can lead to life-threatening complications ranging from perforation to toxic megacolon20. Therefore, 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 operation22, and that the loss or overexpression of 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 autophagy22,23. In many epidemiological studies, it is stated that there is a relationship between vitamin D3 levels and the life quality of IBD patients22. It has been observed that supplementing vitamin D in patients with active UC with low level of vitamin D decreases the clinical activity of the disease, decreases the levels of inflammation markers and improves histopathological alterations24. Vitamin D plays a role in cell proliferation and differentiation, as well as immunomodulation25,26. The vitamin D supplementation in the treatment of some immune-related diseases is increasing. However, there is not sufficient information on the efficacy of its use in acute colitis treatment. In this study, our objective was to determine the efficacy of biochemical and histological changes in rats by giving vitamin D in acute colitis model, which is induced by acetic acid in a rat model. Our results showed that vitamin D inhibited not only oxidant damage but also inflammatory cytokines and histologically improved the colonic inflammation induced by AA in rats. This study suggests that vitamin D is an effective anti-inflammatory and antioxidant and that it may be a promising therapeutic option for ulcerative colitis. However, there is a need for more detailed studies in order to assess the possible relationships between colitis induced with acetic acid and vitamin D. Source: http://doi.org/10.1590/s0102-865020200040000004