Biomedical subjects
Publications and source records attributed to H Tsujibo.
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We examined the inhibitory activities of branched-chain fatty acids of iso-C12:0 to iso-C16:0 on gastric secretion in rats. Consequently, iso-C13:0 and iso-C15:0 were found to have strong inhibitory activities on gastric secretion in rats. In the case of intraduodenal administration, iso-C15:0 also showed a significant inhibition of gastric juice secretion. Therefore, the effects of iso-C13:0 and iso-C15:0 on ulceration in pylorus-ligated rats and aspirin-induced ulcer were examined. At the doses of 10 and 25 mg/kg, iso-C13:0 and iso-C15:0 significantly decreased the ulcer index in pylorus-ligated rats, and aspirin-induced ulcer was also significantly inhibited at the doses of 25 and 50 mg/kg. Finally, effect of iso-C15:0 on pepsin, Mg++-ATPase and carbonic anhydrase, which are considered to play an important role in the mechanism of gastric juice secretion, was examined in vitro, centering around iso-C15:0 which showed a marked effect in gastric juice secretion inhibitory and anti-ulcerogenic activities. Iso-C15:0 showed inhibitory activity on pepsin and Mg++-ATPase, but entirely no activity on inhibiting carbonic anhydrase.
Fatty acids of C10:0, C12:0, C13:0, C14:0 and C16:0 significantly inhibited the amount of gastric juice, total acid output, and total peptic activity, but fatty acids of C17:0-C20:0 entirely failed to show significant inhibitory activity. Only the methyl ester of C14:0 showed significant inhibition of these parameters at the dose of 100 mg/kg, while at the dose of 200 mg/kg, methyl esters of fatty acids of fatty acids of C10:0, C12:0, C14:0, and C16:0 significantly inhibited these three parameters. alpha-Monoglyceride of C14:0 significantly inhibited the amount of gastric juice at the dose of 100 mg/kg, while alpha-monoglycerides of C10:0, C12:0', C13:0, C14:0, and C16:0 significantly inhibited the amount of gastric juice, total acid output, and total peptic activity at the dose of 200 mg/kg. In the case of intraduodenal administration, myristic acid also showed significant inhibition of these parameters at 100 and 200 mg/kg doses. The dose-activity correlation in gastric secretion inhibitory activity was examined with myristic acid and this activity was found to increase with increasing dose of the acid administered. Myristic acid significantly decreased the ulcer index in aspirin-induced ulcer, it was entirely ineffective in preventing histamine-induced ulcer. Finally, inhibitory effect of myristic acid on pepsin and histidine decarboxylase was examined in vitro and it was found that myristic acid inhibited peptic activity, but it had almost no effect of inhibiting the histidine decarboxylase activity.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.