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In vivo effect of diallyl sulfide and cimetidine on phenacetin metabolism and bioavailability in rat

100%
Szutowski M. M., Zalewska K., Jadczak M., Marek M.
Acta Biochimica Polonica
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2002
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tom 49
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nr 1
Numerous cytochrome P450 inhibitors have been described as effective modulators of cytochrome P450 isoforms activity in vitro. Their inhibitory efficiency may be con­siderably modified after in vivo application. The aim of this study was to examine the effect of oral administration of diallyl sulfide — a cytochrome P450 2E1 inhibitor and cimetidine — a cytochrome P450 2C6 and 2C11 inhibitor on rat serum concentration of phenacetin and its metabolite acetaminophen. Both inhibitors increased area un­der the curve (AUC0-4h) for phenacetin by 50%. Only cimetidine reduced AUC0-4 h for acetaminophen indicating inhibition of O-deethylation activity. Quinidine — a cyto­chrome P450 2D subfamily and P-glycoprotein inhibitor did not change significantly phenacetin bioavailability. These results suggest that diallyl sulfide inhibits the deacetylation pathway catalysed by arylamine N-acetyl transferase. Beside cyto­chrome P450 1A2 other cytochrome P450 isoforms (2A6 and/or 2C11) are involved in phenacetin O-deethylation in rat.
2
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Comparison of prostaglandin and cimetidine in protection of isolated gastric glands against indomethacin injury

84%
Brzozowski T., Tarnawski A., Hollander D., Sekhon S., Krause W. J., Gergely H.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
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nr 5
75-88
Prostaglandins can protect the in vivo gastric mucosa against necrosis produced by a variety noxious agents. Cimetidine has also been shown to have protective properties in humans and in some models of experimental injury. Whether prostaglandins or cimetidine may protect gastric mucosal cells directly in the absence of systemic factors remains controversial. In the present study, the potential protective actions of prostaglandin and cimetidine against indomethacin injury were assessed in isolated rat gastric glands. Gastric glands were pre-incubated in oxygenated medium with either placebo, 16,16 dimethyl prostaglandin E2 (dm PGE2) or cimetidine and incubated at 37°C in medium containing 0.5 mg/ml of indomethacin for 2, 4 and 6 hrs. Cell injury and protection was assessed by the Fast Green exclusion test (viability test), leakage of lactate dehydrogenase (LDH) into the medium, and by scanning and transmission electron microscopy. In addition, the generation of PGE2 by the gland cells was determined using RIA assay. Indomethacin by itself significantly reduced the viability of gastric glands, increased LDH release into the medium and produced prominent ultrastructural damage. In contrast to cimetidine, co-incubation of gastric glands with dm PGE2 added to indomethacin, significantly reduced indomethacin-induced injury, increased the number of viable cells, reduced LDH leakage and diminished the extent of ultrastructural damage. The dose of indomethacin (5 µg/ml) which significantly inhibited the generation of PGE2 (up to 90% inhibition) had no effect on cell viability nor LDH release. We conclude that 1) exogenous PGE2 exerts a potent protective activity in vitro which is independent on neural, vascular and hormonal factors; 2) inhibition of endogenous PGs may not the primary mechanism in the deleterious action of indomethacin against damage to gastric glandular cells and 3) indomethacin can exert a direct cytotoxic effect on the mucosal cells in gastric glands.
3
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The effect of PGF2 alpha-estrumate on the secretion and composition of abomasal juice in sheep during H2-histaminic receptor blockade with cimetidine

84%
Dejneka J., Lukaszewska J., Paradowski L., Zalucki G.
Acta Physiologica Polonica
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1987
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tom 38
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nr 4
4
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A histamine H2 receptor antagonist, roxatidine, stimulates mucus secretion and synthesis by cultured rabbit gastric mucosal cells

67%
Takahashi S., Okabe S.
Journal of Physiology and Pharmacology
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1995
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tom 46
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nr 4
5
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A new ulcer model unhealed gastric ulcers, induced by chronic treatment with indomethacin in rats with acetic acid ulcers

67%
Amagase K., Okabe S.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 2
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