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

The Japanese Journal of Pharmacology

Kunihiro Odaguchi¹  Takuji Mizui¹  Yozo Hori¹  Kiyoshi Yasui¹  Hirokuni Jyoyama¹ 

[1] Division of Pharmacology, Discovery Research Laboratoris II Shionogi & Co., Ltd.

关键词: Benexate hydrochloride betadex;    Gastric mucosa;    Indomethacin;    Prostaglandin;    Pleurisy;   

DOI  :  10.1254/jjp.72.183

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(31)Cited-By(2)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 indomethacintreated 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.

【 授权许可】

Unknown