GERANYLGERANYLACETONE AND CETRAXATE HYDROCHLORIDE INCREASE UDP-GALACTOSYLTRANSFERASE ACTIVITY IN RAT GASTRIC-MUCOSA

Citation
Y. Mikami et al., GERANYLGERANYLACETONE AND CETRAXATE HYDROCHLORIDE INCREASE UDP-GALACTOSYLTRANSFERASE ACTIVITY IN RAT GASTRIC-MUCOSA, Acta medica Okayama, 51(5), 1997, pp. 245-249
Citations number
25
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
0386300X
Volume
51
Issue
5
Year of publication
1997
Pages
245 - 249
Database
ISI
SICI code
0386-300X(1997)51:5<245:GACHIU>2.0.ZU;2-6
Abstract
UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoprotein which plays an important role in gastric mucosa l defensive mechanisms. Analysis of gastric UDP-Gal-T activity should clarify the mechanisms of the action of antiulcer drugs regarding gast ric defensive factors. Here, we examined UDP-Gal-T activity in rat gas tric mucosa treated with the antiulcer drugs geranylgeranylacetone (GG A) and cetraxate hydrochloride (CET). The effects of coadministration of indomethacin and exogenous administration of prostaglandins (PGs) w ere also studied. GGA and CET significantly increased UDP-Gal-T activi ty, and coadministration of indomethacin inhibited the increase of enz yme activity. UDP-Gal-T activity level with GGA was significantly high er than the control level, even in the presence of indomethacin. With CET, however, this was not the case. Among PGs, PGE(1) significantly i ncreased enzyme activity. Concomitant administration of PGE(1) and GGA or CET increased UDP-Gal-T activity even with indomethacin to the lev els achieved when these antiulcer drugs were administered without indo methacin. Our findings suggest that GGA and CET exert antiulcer effect s by increasing mucus glycoprotein synthesis and that endogenous PG sy nthesis may be involved in this process. However, mechanisms not media ted by endogenous PGs may also exist in the stimulatory action of GGA on UDP-Gal-T activity.