title: [Role of cyclooxygenase in modification of intestinal microflora under stress condition].
abstract: Stress and nonsteroidal anti-inflammatory drugs, which act as nonselective inhibitors of cyclooxygenase, are the main factors of ulcerogenesis in digestive system. However, the peculiarities of their combined action upon the status of intestinal microflora and the parameters of NO-synthase system are still poorly understood. In experiments with rats we show that water-restrained stress was accompanied by a considerable increase of iNOS activity and intensity of lipoperoxidation processes. The increase of Escherichia coli content and the decrease in Enterococcus spp. concentration in the small intestine with their simultaneous rise in the large intestine were noticed under these conditions. Cyclooxygenese blockage with naproxen prior to induction of water-restrained stress was accompanied by the decease of iNOS in small and large intestines, with the synchronous rise of cNOS activity in the large intestine as compared with indexes in stress. The moderate increase in Enterococcus spp. content in duodenum with the rise of Escherichia coli concentration in the ileum was shown. The Escherichia coli content decreased in the proximal part of the large intestine and decreased in its distal part. Disbiosis, intensification of lipoperoxidation processes and changes in NO-synthase system parameters under condition of simultaneous action of stress and cyclooxygenase blockage can create preconditions for the development of destructive changes and enteropathias.
authors.forename: I S
authors.initials: IS
authors.lastname: Fomenko
authors.forename: O P
authors.initials: OP
authors.lastname: Korniychuk
authors.forename: A R
authors.initials: AR
authors.lastname: Hural
authors.forename: R G
authors.initials: RG
authors.lastname: Shykula
authors.forename: I I
authors.initials: II
authors.lastname: Ilkiv
authors.forename: A Ya
authors.initials: AY
authors.lastname: Sklyarov
mesh_terms: D000818:Animals; D021461:Animals, Outbred Strains; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D064806:Dysbiosis / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D016983:Enterococcus / Q000254:growth & development; D004926:Escherichia coli / Q000254:growth & development; D007413:Intestinal Mucosa / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D007420:Intestine, Large / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D007421:Intestine, Small / Q000201:enzymology / Q000382:microbiology* / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D009288:Naproxen / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D051381:Rats; D013312:Stress, Physiological; D014868:Water Deprivation
chemical_list: D016861:Cyclooxygenase Inhibitors; D009569:Nitric Oxide; D009288:Naproxen; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D011451:Prostaglandin-Endoperoxide Synthases