Inhibition of prostaglandin biosynthesis by a new anti-inflammatory drug, TA-60.
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 PGE2 biosynthesis of the bovine seminal vesicle microsome dose-dependently. The inhibition constant (Ki) of TA-60 was approximately 8 microM. 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 PGE2 biosynthesis unlikely to indomethacin (IM). The decrease in the PGE2 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 PGE2 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 PGE2.[1]References
- Inhibition of prostaglandin biosynthesis by a new anti-inflammatory drug, TA-60. Muramatsu, M., Tanaka, M., Fujita, A., Otomo, S., Aihara, H., Amano, T. J. Pharmacobio-dyn. (1985) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
