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Results for “AMINOSALICYLIC ACID”

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PubMed1999

Aminosalicylic acid inhibits IkappaB kinase alpha phosphorylation of IkappaBalpha in mouse intestinal epithelial cells.

Tumor necrosis factor alpha (TNFalpha)-stimulated nuclear factor (NF) kappaB activation plays a key role in the pathogenesis of inflammatory bowel disease (IBD). Phosphorylation of NFkappaB inhibitory protein (IkappaB) leading to its degradation and NFkappaB activation, is regulated by the multimeric IkappaB kinase complex, including IKKalpha and IKKbeta. We recently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation and NFkappaB activation. To determine the mechanism of 5-ASA inhibition of IkappaB degradation, we studied young adult mouse colon (YAMC) cells by immunodetection and in vitro kinase assays. We show 5-ASA inhibits TNFalpha-stimulated phosphorylation of IkappaBalpha in intact YAMC cells. Phosphorylation of a glutathione S-transferase-IkappaBalpha fusion protein by cellular extracts or immunoprecipitated IKKalpha isolated from cells treated with TNFalpha is inhibited by 5-ASA. Recombinant IKKalpha and IKKbeta autophosphorylation and their phosphorylation of glutathione S-transferase-IkappaBalpha are inhibited by 5-ASA. However, IKKalpha serine phosphorylation by its upstream kinase in either intact cells or cellular extracts is not blocked by 5-ASA. Surprisingly, immunodepletion of cellular extracts suggests IKKalpha is predominantly responsible for IkappaBalpha phosphorylation in intestinal epithelial cells. In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activity toward IkappaBalpha in intestinal epithelial cells. These findings suggest a novel role for 5-ASA in the management of IBD by disrupting TNFalpha activation of NFkappaB.

Animals↗
PubMed2006

A two-stage decision analysis to assess the cost of 5-aminosalicylic acid failure and the economics of balsalazide versus mesalamine in the treatment of ulcerative colitis.

Ulcerative colitis (UC) is a costly disease, especially if not properly treated. Epidemiologic studies have shown that many patients progress in one year from initial treatment with prednisone to expensive colonectomy surgery if the UC is not managed with drug therapy. A two-stage decision analysis was conducted to (1) estimate the cost of a 5-aminosalicylic acid (5-ASA) treatment failure using the treatment guidelines recommended by the American College of Gastroenterology and (2) incorporate the cost of a 5-ASA treatment failure to determine which oral 5-ASA agent results in cost minimization and cost effectiveness. The analysis was conducted from the payer perspective, incorporating results from clinical trials directly comparing oral balsalazide capsules and a specific formulation of oral mesalamine. Health care costs related to UC for an oral 5-ASA failure is greater than dollar 11,500 on average in the first six months after therapy. Patients treated with balsalazide capsules had 16% lower total direct health care costs, 32% better outcomes (days without symptoms or steroids), and 37% greater cost effectiveness compared with patients treated with a specific formulation of oral mesalamine. Coordinated efforts should be taken to avoid the cost and morbidity associated with 5-ASA treatment failures.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Oxazolone-induced colitis in rats: effects of budesonide, cyclosporin A, and 5-aminosalicylic acid.

BACKGROUND: The intention of the present study was to develop a new hapten-based inflammatory bowel disease model in the rat, useful for pharmacologic screening of new substances with anti-inflammatory properties and immunomodulating capacities. It was considered important to avoid the use of an irritating barrier breaker, such as ethanol. METHODS: Dark Agouti rats were skin-sensitized with oxazolone and further challenged intra-rectally with oxazolone dissolved in carmellose sodium (Orabase)/peanut oil. The effects of treatment with budesonide, prednisolone, cyclosporin A, and 5-aminosalicylic acid (5-ASA) were studied. RESULTS: The intra-rectal challenge with oxazolone in sensitized rats induced an inflammation with an increased colon wet weight, pronounced myeloperoxidase (MPO) activity, and hyperemia/ulcerations in the epithelial lining. Improvement was achieved by treatment with budesonide, prednisolone, and cyclosporin A but not with 5-ASA. CONCLUSIONS: The model fulfills the criteria for a fast, reproducible animal model for human colon inflammation, suitable for pharmacologic screening and studies of an immune-driven colon inflammation.

Animals↗