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It is well-known that prostaglandin (PG) synthetase inhibitors such as aspirin and indomethacin induce gastrointestinal ulcer both in experimental animals and humans. In addition, it has been reported that PG levels in the plasma and gastric juice of patients with ulcer are significantly lower than these levels in healthy subjects (1). On the other hand, PGE type PGs and their analogs are effective against experimental ulcer produced in animals (2-6). These results suggest that stimulants of PG synthetase may prevent ulceration in the gastrointestinal mucosa and repair an already formed ulcer. We attempted to determine whether the stimulation of PG biosynthesis in vitro by hydroxyphenyl alkanoic acids cor relates with anti-ulcerogenic activity of the acids in the rat. PG synthetase activity was assayed according to the method of Tachizawa et al. (7) in the following incubation mixture at 37°C for 30 min: 7.5 mg of lyophilized microsomes of the rabbit renal medulla, 301M 3H-arachidonic acid, 1.7 mM reduced 1-glutathione, 0.07 mM EDTA-2Na and 1 mM hydroxyphenyl alkanoic acids or reference compound, 0.5 mM l-epinephrine bitartrate, in 1.5 nil of 0.2 M Tris-HC1 buffer (pH 7.5). PGs formed from the substrate were extracted and separated by TLC and the radioactivity of each spot on the TLC plate was measured by a liquid scintillation counter. Percent increase was obtained by comparing the percentage of radioactivity converted from the labeled substrate into PGE2 with or without hydroxyphenyl alkanoic acids or /-epinephrine. Anti-ulcerogenic activity of hydroxyphenyl alkanoic acids was expressed as percent inhibition against aspirin-induced gastric ulcer. Seven male Sprague-Dawley rats weighing 106 to 148 g, (Charles River), were fasted overnight. Aspirin was administered p.o. to the animals at a dose level of 200 mg/kg in a suspension of 0.5 % carboxymethyl cellulose solution and 3.5 hr later the animals were sacrificed. The stomachs were removed and examined macroscopically for gastric ulcer. Ulcer index was expressed as sum of the length of each lesion. Test compounds (250 mg,/kg) were given p.o. it a suspension of 0.5 °% carboxymethyl cellulose solution 1 hr before the aspirin administration. Compounds tested were as follows: p-hydroxybenzoic acid (I), 5-hydroxypyridine-2-carboxylic acid (1I), 3,4,5-trihydroxybenzoic acid (III), p-hydroxyphenylacetic acid (IV), 3-(p-hydroxyphenyl)propionic acid (V), 3-(nt hydroxyphenyl)prop ionic acid (VI), 3-(o-hydroxyphenyl)propionic acid (VII), phenyl propionic acid (VIII), 3-(p-methoxyphenyl)propionic acid (IX), 3-(3,4-dihydroxyphenyl) propionic acid (X), 4-(p-hydroxyphenyl)butylic acid (XI), 6-(p-hydroxyphenyl)hexanoic acid (XII), 3-(p-hydroxyphenoxy)propionic acid (XIII).

CORRELATION BETWEEN THE STIMULATION OF PROSTAGLANDIN BIOSYNTHESIS BY H YD ROXY PHENYL ALKANOIC ACIDS AND THEIR ANTI-ULCEROGENIC ACTIVITY