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1

Exogenous leptin does not affect exocrine pancreatic secretion in conscious sheep

100%
Korczynski W., Kirat D., Kato S.
Journal of Animal and Feed Sciences. Supplement
|
2004
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tom 13
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nr 1
2
Content available remote

Role of endothelial nitric oxide synthase in aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats

88%
Kato S., Ohkawa F., Ito Y., Amagase K., Takeuchi K.
Journal of Physiology and Pharmacology
|
2009
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tom 60
|
nr 4
147-155
The role of nitric oxide synthase (NOS) isozymes in the aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats was investigated. Two weeks after injection of Freund’s complete adjuvant, the animals were given indomethacin, and the stomach was examined for damage 4 h later. Indomethacin caused hemorrhagic lesions in the normal rat stomach, and these lesions were markedly aggravated in arthritic rats. Pretreatment with L-NAME (a nonselective inhibitor of NOS) and aminoguanidine (a relative selective inhibitor of iNOS) did not affect the ulcerogenic response in normal rats but dose-dependently prevented the aggravation of lesions in arthritic rats, but the effect of aminoguanidine was apparently less than that of L-NAME. The increased ulcerogenic response in arthritic rats was significantly suppressed by 1400 W (a selective inhibitor of iNOS) and L-NIO (a selective inhibitor of eNOS) but not by L-NPA (a selective inhibitor of nNOS). The concurrent administration of 1400 W and L-NIO almost totally abolished the aggravation of damage in arthritic rats. The expressions of eNOS and iNOS but not nNOS in the gastric mucosa were clearly enhanced in arthritic rats. Mucosal levels of non-protein sulfhydryls were significantly lower in arthritic rats than those in normal rats. The aggravation of damage in arthritic rats was significantly prevented by glutathione. These results suggest that the increased ulcerogenic response to indomethacin in arthritic rat stomachs is mediated by NO derived from eNOS in addition to iNOS. It is assumed that eNOS/NO may act harmfully on the gastric mucosa of arthritic rats with mucosal SH deficiency.
3

Monocarboxylate transporter 1 (MCT1) in calf and sheep stomach

88%
Kirat D., Inoue H., Iwano H., Yokota H., Kato S.
Journal of Animal and Feed Sciences. Supplement
|
2004
|
tom 13
|
nr 1
4

The effect of exogenous leptin on pancreatic enzyme secretion in anaesthetized rats

88%
Matyjek R., Wolinski J., Laubitz D., Kato S., Zabielski R.
Journal of Animal and Feed Sciences
|
2005
|
tom 14
|
nr 2
5
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Content available

Dual action of nitric oxide in pathogenesis of indomethacin-induced small intestinal ulceration in rats

88%
Tanaka A., Kunikata T., Mizoguchi H., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 3
6
Content available remote

Role of macrophage colony-stimulating factor (M-CSF)-dependent macrophages in gastric ulcer healing in mice

76%
Kawahara Y., Nakase Y., Isomoto Y., Matsuda N., Amagase K., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 4
7
Content available remote

Dual role of endogenous nitric oxide in development of dextran sulfate sodium-induced colitis in rats

76%
Rumi G., Tsubouchi R., Nishio H., Kato S., Mozsik G., Takeuchi K.
Journal of Physiology and Pharmacology
|
2004
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tom 55
|
nr 4
The role of nitric oxide (NO) in the etiology of ulcerative colitis is controversial with reports of the improvement and aggravation of colonic lesions by inducible NO synthase (iNOS) inhibitors. In the present study, we compared the effect of the selective iNOS inhibitor aminoguanidine and the nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on a dextran sulfate sodium (DSS)-induced model of colitis in rats. Experimental colitis was induced by a 3% DSS-solution added to drinking water for 7 days. Aminoguanidine (5~20 mg/kg) and L-NAME (10 mg/kg) were administered p.o. twice daily for the first 3 days, the last 3 days or all 6 days of DSS treatment. Body weight and severity of colitis (diarrhea, bloody feces) were observed over a period of 7 days. DSS treatment resulted in severe colonic lesions, accompanied by diarrhea, bloody feces, decrease of body weight and colon shortening. All of the parameters investigated improved significantly with aminoguanidine treatment at 20 mg/kg for 6 days or the last 3 days of DSS-treatment, but L-NAME did not significantly affect the colitis during these periods. When L-NAME or aminoguanidine was given in the first 3 days of DSS treatment, the colonic lesions were slightly aggravated by L-NAME but not affected by aminoguanidine. The expression of iNOS mRNA was observed from the 3rd day of DSS treatment. These results suggested that endogenous NO exerts a biphasic influence on DSS-induced colitis, depending on the NOS isoenzyme; a beneficial effect of NO derived from constitutive NOS and a detrimental effect of NO produced by iNOS in the development of colitis.
8
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Content available

Ulcerogenic and healing impairing actions of monochloramine in rat stomachs: effects of zinc L-carnosine, polaprezinc

76%
Nishiwaki H., Kato S., Sugamoto S., Umeda M., Morita H., Yoneta T., Takeuchi K.
Journal of Physiology and Pharmacology
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1999
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tom 50
|
nr 2
9
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Content available

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

76%
Konaka A., Nishijima M., Tanaka A., Kunikata T., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
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1999
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tom 50
|
nr 1
10
Content available remote

Roles of nitric oxide (NO) and NO synthases in healing of dextran sulfate sodium-induced rat colitis

76%
Aoi Y., Terashima S., Ogura M., Nishio H., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
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2008
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tom 59
|
nr 2
We examined the effects of various NO inhibitors on the healing of DSS-induced rat colitis. Experimental colitis was induced by feeding rats for 6 days with 2.5% DSS in drinking water. After DSS treatment, the animals were fed normally and killed various days up to 7 days later. L-NAME (a nonselective NOS inhibitor) or aminoguanidine (a selective iNOS inhibitor) was given p.o. twice daily for 6 days starting from the termination of DSS treatment. The area of lesions, colon length and MPO activity were measured on day 7 after DSS treatment. DSS treatment caused severe lesions in the colon, accompanied by an increase in MPO activity and a decrease in colon length. The lesions healed gradually after discontinuation of DSS treatment, with a histological restoration and subsidence of inflammation. The healing of DSS-induced colonic lesions was significantly impaired by daily administration of L-NAME or aminoguanidine, the effects being all but equivalent between these drugs, and the effect of L-NAME was significantly reverted by the co-administration of L-arginine. The expression of nNOS protein was observed in the colonic mucosa with or without DSS treatment, while those of iNOS and eNOS were markedly upregulated after DSS treatment. Likewise, the expression of VEGF was also up-regulated in the colon following DSS treatment, and this response was suppressed by both L-NAME and aminoguanidine. These results suggest that endogenous NO produced by mainly iNOS and partly eNOS contributes to the healing of DSS-induced colonic lesions, through the upregulation of VEGF expression and enhancement of angiogenesis.
11
Content available remote

Prevention by lansoprazole, a proton pump inhibitor, of indomethacin-induced small intestinal ulceration in rats through induction of heme oxygenase-1

64%
Yoda Y., Amagase K., Kato S., Tokioka S., Murano M., Kakimoto K., Nishio H., Umegaki E., Takeuchi K., Higuchi K.
Journal of Physiology and Pharmacology
|
2010
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tom 61
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nr 3
287-294
The effect of lansoprazole, a proton pump inhibitor (PPI), on indomethacin-induced small intestinal ulceration was examined in rats, particularly in relation to heme oxygenase (HO)-1. The animals were administered indomethacin (10 mg/kg, p.o.) and killed 24 h later. Lansoprazole (30-100 mg/kg, p.o.) and omeprazole (30-100 mg/kg, p.o.) were given 30 min before the administration of indomethacin, while tin-protoporphyrin IX (SnPP: 30 mg/kg, i.v.), an inhibitor of HO-1, was injected 10 min before indomethacin or lansoprazole. Indomethacin produced hemorrhagic lesions in the small intestine, accompanied with an increase of mucosal invasion of enterobacteria, inducible nitric oxide synthase (iNOS) expression, and myeloperoxidase (MPO) activity in the mucosa. Pretreatment with lansoprazole dose- dependently reduced the severity of the indomethacin-induced intestinal lesions, with suppression of the increased MPO activity, while omeprazole had no effect. Pretreatment with SnPP significantly exacerbated these intestinal lesions and almost totally abolished the protective effect of lansoprazole. The up-regulation of iNOS mRNA expression following indomethacin was suppressed by lansoprazole in a SnPP-inhibitable manner, although the enhanced enterobacterial invasion remained unaffected. The amount of HO-1 protein in the intestinal mucosa was significantly increased by lansoprazole but not by omeprazole. Prior administration of carbon monoxide (CO)-releasing molecule-2 (CORM-2; 10 mg/kg, i.p.) significantly reduced the severity of these lesions and the enhancement of mucosal iNOS mRNA expression induced in the small intestine by indomethacin. These results suggest that lansoprazole prevents indomethacin-induced small intestinal ulceration, and this effect is associated with inhibition of iNOS expression, through up-regulation of HO-1/CO production in the mucosa.
12
Content available remote

Lafutidine, a histamine H2 receptor antagonist with mucosal protective properties, attenuates 5-fluorouracil-induced intestinal mucositis in mice through activation of extrinsic primary afferent neurons

64%
Sano T., Utsumi D., Amagase K., Matsumoto K., Tominaga M., Higuchi K., Takeuchi T., Kato S.
Journal of Physiology and Pharmacology
|
2017
|
tom 68
|
nr 1
13
Content available remote

Phosphodiesterase isozymes involved in regulating acid secretion in the isolated mouse stomach

64%
Okuda S., Honda M., Ito Y., Aihara E., Kato S., Mitsufuji S., Yoshikawa T., Takeuchi K.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 7
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