Effects of sofalcone on necrotizing agents-induced gastric lesions and on endogenous prostaglandins in rats stomachs.

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Abstract
Attempts was made to investigate the effect of 2''-carboxymethoxy-4,4''-bis(3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o. [per os] markedly suppressed 0.6 N HCl- or 100% EtOH [Etanol]-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2 N NaOH-induced gastric lesions. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and i.p. routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 0.6 N HCl-induced gastric lesions were significantly aggravated by indomethacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. PG-like activity in the gastric tissue was increased in both the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach.