Abstract
Purpose To examine the therapeutic effect of external adenosine on an acetic acid-induced acute ulcerative colitis model in rats.Methods Thirty male mature rats were divided into three groups as control, acute colitis (AC) and AC+adenosine group (AC+AD). AC was induced by rectal administration of 4% acetic acid (AA). 5mg/kg/day adenosine was performed i.p for 4 weeks to AC+AD group. Rectum and colon were excised for microscopic and histopathological histopathologic evaluations, and immunohistochemical analysis of nuclear factor kappa B (NF-kB). Blood samples were collected for biochemical detection of TNF-α, Pentraxin-3 and malondialdehyde (MDA) levels.Results AC group had generalized hyperemia and hemorrhage with increased macroscopic and histopathological scores compared with control (P <0.0001) while adenosine treatment decreased these scores significantly (P <0.001), with reduced distribution of disrupted epithelium, leukocyte infiltrates, and focal hemorrhage. AC group showed significantly increased immunoexpression of NF-kB in rectum, plasma and tissue levels of TNF-α, plasma Pentraxin-3 and MDA levels (P <0.0001) while adenosine reduced these levels (P < 0.05).Conclusion Adenosine appears to promote healing of colon and rectum exposed to AA-induced AC, suggesting a boosting effect of adenosine on the intestinal immune system to cure ulcerative colitis.
Highlights
Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal tract
All animals (n=30) in this 4 week-study survived at the end of procedures and there was no need to exclude none due to any inflammation or any alteration in feeding or weighing or complication of application by acetic acid or anesthesia protocol
Microscopic evaluation showed that the acute ulcerative colitis was successfully induced by 4% acetic acid (AA) in 20 rats (Fig. 1)
Summary
Ulcerative colitis is a chronic inflammatory disease of the gastrointestinal tract. Its etiology involves the basic clinical symptoms of rectal bleeding, diarrhea, weight loss and abdominal pain, and other signs include anemia, fever, joint pain, damage to mucus membranes, renal calculi, and osteoporosis[1,2]. Some alternative approaches have been recommended for ulcerative therapy, such as transdermal administration of nicotine, omega-3 fatty acids with anti-inflammatory properties, and biological substances, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-2 receptor, and anti-IL-12 and IL-6 antibodies[5,6,7], and even experimental treatments with the flavonoid compounds such as quercetin[8] and hawthorn-derived products found in plant extracts[9] Despite this great deal of attention in the therapeutic approaches to the disease during the past years, the pharmacological treatment is still unsatisfactory[3]
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