ArticleDigestive diseases and sciences2008
5-aminosalicylic acid improves indomethacin-induced enteropathy by inhibiting iNOS transcription in rats.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular Mechanisms of the Antitumor Effects of Mesalazine and Its Preventive Potential in Colorectal Cancer.Molecules (Basel, Switzerland) · 2023Review
- Chemoprevention of Colitis-Associated Dysplasia or Cancer in Inflammatory Bowel Disease.Gut and liver · 2022Review
- Cell-free probiotic supernatant (CFS) treatment alleviates indomethacin-induced enterocolopathy in BALB/c mice by down-modulating inflammatory response and oxidative stress: potential alternative targeted treatment.Inflammopharmacology · 2022Article
- The Protective Effect of 5-Aminosalicylic Acid Against Non-Steroidal Anti-Inflammatory Drug-Induced Injury Through Free Radical Scavenging in Small Intestinal Epithelial Cells.Medicina (Kaunas, Lithuania) · 2020Article
- The Serum S100B Level as a Biomarker of Enteroglial Activation in Patients with Ulcerative Colitis.International journal of inflammation · 2014Article
- TNF-alpha modulates iNOS expression in an experimental rat model of indomethacin-induced jejunoileitis.Molecular and cellular biochemistry · 2010Article
- 5-aminosalicylic acid improves indomethacin-induced enteropathy by inhibiting iNOS transcription in rats.Digestive diseases and sciences · 2008Article
- Inhibition of TNF-alpha improves indomethacin-induced enteropathy in rats by modulating iNOS expression.Digestive diseases and sciences · 2005Article
- Chemoprophylaxis of precancerous lesions in patients who are at a high risk of developing colorectal cancer (Review).Medicine internationalReview
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide has been implicated in the pathogenic mechanism of inflammatory bowel disease states. We evaluated indomethacin-induced enteropathy in rats, in relation to the expression of the inducible isoform of NO synthase (iNOS) using aminosalicylic acid (5-ASA), its isomer 4-ASA (10 or 50 mg/kg/day, po), and dexamethasone, an iNOS transcription inhibitor (3 mg/kg/day, sc). Enteropathy was induced by indomethacin (7.5 mg/kg/day, sc) for two days and the small intestine was examined for lesions over the next 14 days. Indomethacin-induced small-intestinal ulcer size, mucosal myeloperoxidase activity, iNOS expression and serum nitrite/nitrate levels were maximally increased by day 4 and gradually decreased by day 14. Treatment with 5-ASA, but not 4-ASA, decreased indomethacin-induced ulcer length, myeloperoxidase activity, serum nitrite/nitrate levels and iNOS expression at day 4. Dexamethasone had a greater effect than 5-ASA in reducing myeloperoxidase activity and ulcer length by 26 and 32%, respectively. Dexamethasone also reduced serum nitrate/nitrite and iNOS expression to their basal levels. In conclusion, inhibition of iNOS expression by 5-ASA appears to be associated with diminished intestinal ulceration in indomethacin-induced enteropathy.
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