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Abstract
Objective: This study targets the inhibition of inflammatory mediators and the enhancement of gastrointestinal mucosa healing in ulcerative colitis in rats through sulfasalazine. Methods: Twenty four female albino rats were divided into 3 groups: normal control, colitis group (rats received 5% dextran sodium sulfate (DSS) in their drinking water for 7 d), sulfasalazine group (500 mg/kg/day was administrated orally one week ahead of DSS and parallel with its administration). The impact of sulfasalazine on intestinal inflammation was investigated via estimation of some inflammatory mediators, namely; serum Leucine rich α 2 Glycoprotein (LRG) as well as colon cAMP, Myloperoxidase (MPO) and TNF-α using ELISA technique as well as gene expression of Trefoil Factor 3 (TFF3), High mobility group box1 (HMGB1), Nuclear factor kappa B (NF-κB) and metalloproteinase-3 (MMP3) and miRNA-31 levels using RT-PCR. Results: Sulfasalazine substantially decreases the release of LRG, MPO and TNF-α and the expression of HMGB1, NF-κB, MMP3, TFF3 and miRNA31 at p≤ 0.05 compared to colitis group in vivo. Moreover, Sulfasalazine significantly increases the colonic cAMP at p≤ 0.05 in groups of rats treated with DSS. Conclusion: Sulfasalazine has a protective effect on inflammatory bowel disease causing mucosal healing within the gastrointestinal tract. Additional studies are warranted to explore the molecular mechanism of sulfasalazine in ulcerative colitis and its clinical application.
Highlights
Inflammatory bowel disease (IBD) comprises Crohn’s disease (CD) and ulcerative colitis (UC) is thought to be triggered by an irregular immune response resulting in a genetically prone host malfunction of the intestinal mucosal barrier against enteric bacteria [1]
dextran sodium sulfate (DSS), Sulfasalazine, hexadecyltrimethylammonium bromide (HTAB), O-dianisidine hydrochloride and potassium phosphate buffer were bought from Sigma Aldrich
Treatment with sulfasalazine significantly elevated the level of colonic cAMP level (P
Summary
Inflammatory bowel disease (IBD) comprises Crohn’s disease (CD) and ulcerative colitis (UC) is thought to be triggered by an irregular immune response resulting in a genetically prone host malfunction of the intestinal mucosal barrier against enteric bacteria [1]. The UC is based on the abnormal degradation of the intestinal mucosa due to various reasons; including genetic, environmental, microbial and immune inflammatory mediators [2]. The treatment priorities for IBDs include complication prevention, recovery and rehabilitation of nutritional deficiencies to improve the quality of life of patients. In the treatment of IBDs, the anti-inflammatory drugs include immunosuppressants, biological agents, antibiotics, and drugs to quash inflammatory responses and to alleviate symptoms [3]. A great number of cytokine abnormalities, including proinflammatory and immunoregulatory molecules have been described. In CD, interferongamma (INF)-γ is generated by intestinal CD4+T cells, while interleukin 12 and 18 are released by mucosal macrophages [3]
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