STUDIES ON THE MECHANISM OF ACTION OF CETRAXATE [4-(2-CARBOXYETHYL)PHENYL TRANS-4-AMINOMETHYL CYCLOHEXANECARBOXYLATE HYDROCHLORIDE], A NEW ANTI-ULCER AGENT

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To elucidate mechanisms involved in the anti-ulcer action of cetraxate, the effects of this agent on the ulcer index (UI), fibrinolytic activity (FA) and contents of several connective tissue components in ulcer tissue were examined using aspirin- and acetic acid ulcers in rats. In aspirin ulcer. cetraxate (100 and 300 mg/kg p.o.), like tranexamic acid (500 mg/kg p.o.), ε-aminocaproic acid (500 mg/kg p.o.) and gefarnatc (200 mg/kg p.o.), inhibited both the UI and FA. However, aluminum sucrose sulfate (1000 mg/kg p.o.) was effective only against the UI and L-glutamine (500 mg/kg p.o.) failed to inhibit both parameters. In acetic acid ulcer, following oral, daily × either 5 or 8 administrations, cetraxate (200 and 300 mg/kg), gefarnate (200 mg/kg), aluminum sucrose sulfate (1000 mg/ kg) and L-glutamine (500 mg/kg) were effective on both the UI and FA. Tranexamic acid (500 mg/kg) and ε-aminocaproic acid (500 mg/kg) were ineffective on the UI, although both agents inhibited FA. In acetic acid ulcer, cetraxate induced increases in hexosamine and uronic acid, that is, acid rnucopolysaccharides (AMPS), especially chondroitin sulfate A and -C, whereas L-glutamine and aluminum sucrose sulfate resulted in increases in hexosamine and sialic acid, that is, glycoproteins. From these results, cetraxate may mainly accelerate the ulcer healing by increasing AMPS in ulcer tissue. Moreover, the local anti-FA property of this agent may be also beneficial in treating bleeding ulcers.

STUDIES ON THE MECHANISM OF ACTION OF CETRAXATE [4-(2-CARBOXYETHYL)PHENYL TRANS-4-AMINOMETHYL CYCLOHEXANECARBOXYLATE HYDROCHLORIDE], A NEW ANTI-ULCER AGENT

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