INHIBITION OF PROSTAGLANDIN BIOSYNTHESIS BY A NEW ANTIINFLAMMATORY DRUG, TA-60

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Effect of a new anti-inflammatory drug which has a little ulcer inducing property on gastrointestinal tract, TA-60 (2-[4-(3-methyl-2-butenyl) phenyl] propionic acid), on the prostaglandin (PG) metabolism was investigated. TA-60 inhibited the PGE_2 biosynthesis of the bovine seminal vesicle microsome dose-dependently. The inhibition constant (K_i) of TA-60 was approximately 8 μM. The potency of TA-60 was approximately the same and two times that of ibuprofen (IP) and phenylbutazone (PBZ), respectively. TA-60 did not show the time dependent inhibition of the PGE_2 biosynthesis unlikely to indomethacin (IM). The decrease in the PGE_2 contents in the stomach of the rats by TA-60 reached a plateau and the content was not decreased to less than a certain level. The PGE_2 content of the intestine was not changed by TA-60. TA-60 did not inhibit the activity of the PG degradating enzyme, 15-hydroxy PG dehydrogenase (15-OH-PG-DH) of the gastric mucosa like the other non-steroidal anti-inflammatory drugs (NSAIDs) : IP, PBZ and IM. These results suggest that the slight ulcerating effect of TA-60 on the gastrointestinal tract might be resulted from the small decreasing effect of TA-60 on the gastrointestinal level of PGE_2.
公益社団法人日本薬学会の論文