ArticleJournal of gastroenterology2009
Mast cells are involved in the pathogenesis of indomethacin-induced rat enteritis.
Article in Journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- The PAD4 inhibitor GSK484 diminishes neutrophil extracellular trap in the colon mucosa but fails to improve inflammatory biomarkers in experimental colitis.Bioscience reports · 2025Article
- Protective Effects of Donkey Milk on Ethanol-Induced Gastric Ulcer in Rat.Veterinary medicine and science · 2025Article
- Polysaccharides fromJournal of ginseng research · 2023Article
- Glycomacropeptide Ameliorates Indomethacin-Induced Enteropathy in Rats by Modifying Intestinal Inflammation and Oxidative Stress.Molecules (Basel, Switzerland) · 2020Article
- Sodium alginate ameliorates indomethacin-induced gastrointestinal mucosal injury via inhibiting translocation in rats.World journal of gastroenterology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNonsteroidal antiinflammatory drug (NSAID)-induced enteropathy is clinically very important, but the pathological mechanisms remain unclear. Mast cells have been reported to play an important role in the pathogenesis of indomethacin-induced small intestinal injury. In this study, we investigated the role of mast cells in indomethacin-induced small intestinal injury using mast cell deficiency (Ws/Ws) rat.
methodsWs/Ws rats and control (W+/W+) rats were given indomethacin (15 mg/kg) subcutaneously, and the intestinal mucosal damage was estimated after 24 h.
resultsThe area (mm2) of macroscopic visible lesions, the concentrations of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation, myeloperoxidase (MPO) activity as an index of neutrophil accumulation, and the content of cytokine-induced neutrophil chemoattractant-1 (CINC-1) were significantly increased in indomethacin-treated groups compared with the sham groups. The development of intestinal lesions in response to indomethacin was prevented in Ws/Ws rats compared with W+/W+ rats, together with significant suppression of the increased levels of TBARS, MPO activities, and CINC-1 levels.
conclusionsThese results indicate that mast cells are involved in the pathogenesis of the intestinal mucosal damage induced by indomethacin.
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