Geranylgeranylacetone and cetraxate hydrochloride increase UDP-galactosyltransferase activity in rat gastric mucosa

UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoprotein which plays an important role in gastric mucosal defensive mechanisms. Analysis of gastric UDP-Gal-T activity should clarify the mechanisms of the action of antiulcer drugs regarding gastric defensive factors. Here, we examined UDP-Gal-T activity in rat gastric mucosa treated with the antiulcer drugs geranylgeranylacetone (GGA) and cetraxate hydrochloride (CET). The effects of coadministration of indomethacin and exogenous administration of prostaglandins (PGs) were also studied. GGA and CET significantly increased UDP-Gal-T activity, and coadministration of indomethacin inhibited the increase of enzyme activity. UDP-Gal-T activity level with GGA was significantly higher than the control level, even in the presence of indomethacin. With CET, however, this was not the case. Among PGs, PGE1 significantly increased enzyme activity. Concomitant administration of PGE1 and GGA or CET increased UDP-Gal-T activity even with indomethacin to the levels achieved when these antiulcer drugs were administered without indomethacin. Our findings suggest that GGA and CET exert antiulcer effects by increasing mucus glycoprotein synthesis and that endogenous PG synthesis may be involved in this process. However, mechanisms not mediated by endogenous PGs may also exist in the stimulatory action of GGA on UDP-Gal-T activity.</p

A study on thr effect of Heliobacter pylori to the gastric mucosal defensive mechanism

UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoproteins, which play an important role in gastric mucosal defensive mechanisms. Helicobacter pylori (HP) induces gastritis and peptic ulceers but mechanisms of HP-induced mucosal injury sre not fully understood. To elucidate the mechanism whereby (HP) infection induces gastric mucosal injury, we investigated the effects HP on the gastric mucosal defensive mechanism by measuring UDP-Gal T activies in HGC-27, a mucin-producing gastric caneer cell line, treated with　various HP-relatd materials (sonicated HP, HP culture supernatants, live HP). HP-related materials induced no significant chages in UDP-Gal T activity, but the enzyme increased when we generated a low concentration of ammonia by adding sonicated HP. and urea simultaneousy. In contrast, UDP-Gal-T activity did not increase when we added live HP instead of sonicated HP. Next, we investigated the effects of HP on ethanol-induced injury in the HGC-27 cells. Pretreatment with ammonia of a low concetration significantly protected cells from ethanol-induced injury. In contrast, pretreatment with live HP and urea generated ammonia of the similar concentration but did not protect cells from the injoy. Our findings that HP has an inhibitory effect against adaptive cytoprotection induced by ammonia by inhibiting the induction of UDP-Gal T

Proton pump inhibitor step-down therapy for GERD: A multi-center study in Japan

AIM: To investigate the predictors of success in step-down of proton pump inhibitor and to assess the quality of life (QOL)