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

• 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
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1254/jjp.72.183

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.