Differential Effect of Benexate Hydrochloride Betadex on Prostaglandin Levels in Stomach and Inflammatory Site in Rats

We compared the effects of an anti-ulcer agent, benexate hydrochloride betadex (BHB), on prostaglandin (PG) levels in gastric tissue and inflammatory exudate in untreated and indomethacin-treated rats. BHB (100, 300 and 1000 mg/kg, p.o.) showed dose-dependent inhibition of gastric mucosal lesions in...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1996, Vol.72(2), pp.183-190
Main Authors: Hori, Yozo, Odaguchi, Kumhiro, Jyoyama, Hirokuni, Yasui, Kiyoshi, Mizui, Takuji
Format: Article
Language:English
Subjects:
6-Ketoprostaglandin F1 alpha - metabolism
Animals
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Anti-Ulcer Agents - pharmacology
Benexate hydrochloride betadex
Benzoates - pharmacology
Carrageenan
Dinoprostone - metabolism
Exudates and Transudates - metabolism
Gastric mucosa
Gastric Mucosa - metabolism
Guanidines - pharmacology
Indomethacin
Male
Pleurisy
Pleurisy - chemically induced
Pleurisy - metabolism
Prostaglandin
Prostaglandins - metabolism
Rats
Stomach - drug effects
Stomach Diseases - chemically induced
Stomach Diseases - drug therapy
Stomach Diseases - metabolism
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Summary:We compared the effects of an anti-ulcer agent, benexate hydrochloride betadex (BHB), on prostaglandin (PG) levels in gastric tissue and inflammatory exudate in untreated and indomethacin-treated rats. BHB (100, 300 and 1000 mg/kg, p.o.) showed dose-dependent inhibition of gastric mucosal lesions induced by indomethacin (30 mg/kg, p.o.). Sustained decrease of PGs (PGE2 and 6-keto-PGF1α) in the gastric wall was observed from 0.5 to 6 hr after indomethacin treatment. BHB (300 and 1000 mg/kg) dose-dependently led to recovery of the indomethacin-induced decrease of gastric PGs at 1 and 6 hr after dosing. It did not antagonize the indomethacin-induced decrease of PG levels in the pleural exudate of carrageenin pleurisy nor did it affect the anti-inflammatory effects of indomethacin. BHB (100 to 1000 mg/kg) alone increased gastric PGE2 by 61% to 113%, while it decreased PGE2 levels in the pleural exudate by 9% to 71% at 6 hr after dosing. These results suggest that sustained increase of gastric PGE2 by BHB could be responsible for protection against indomethacin-induced gastric mucosal lesions and that BHB is a suitable anti-ulcer agent for NSAIDs without compromising their anti-inflammatory effects.
ISSN:0021-5198
1347-3506
DOI:10.1254/jjp.72.183