Title : Nitric oxide, superoxide radicals and mast cells in pathogenesis of indomethacin-induced small intestinal lesions in rats.

Pub. Date : 1999 Mar

PMID : 10210152






3 Functional Relationships(s)
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1 These lesions induced by indomethacin were prevented by aminoguanidine (a selective inhibitor of iNOS), dexamethasone (an inhibitor of iNOS mRNA transcription), allopurinol (a xanthine oxidase inhibitor), hydroxyurea (a neutrophil reducing agent) and FR167653 (an inhibitor of interleukin-1/tumor necrosis factor-alpha production) as well as 16,16-dimethyl prostaglandin E2n. Indomethacin nitric oxide synthase 2 Rattus norvegicus
2 These lesions induced by indomethacin were prevented by aminoguanidine (a selective inhibitor of iNOS), dexamethasone (an inhibitor of iNOS mRNA transcription), allopurinol (a xanthine oxidase inhibitor), hydroxyurea (a neutrophil reducing agent) and FR167653 (an inhibitor of interleukin-1/tumor necrosis factor-alpha production) as well as 16,16-dimethyl prostaglandin E2n. Indomethacin nitric oxide synthase 2 Rattus norvegicus
3 These results suggest that: 1) the pathogenic mechanism of indomethacin-induced small intestinal lesions involves superoxide radicals as well as NO produced by iNOS, 2) the deleterious effect of NO may be accounted for by the cytotoxic action of peroxynitrite, produced from NO in the presence of superoxide radicals, and 3) the mast cells may also be involved in the process of small intestinal ulceration, although the mediator responsible remains undefined. Indomethacin nitric oxide synthase 2 Rattus norvegicus