16,16-Dimethyl prostaglandin E2 protects gastric mucosal surface epithelial cells from indomethacin-induced damage in rats.

Abstract

Abstract-The protective effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) against early damage induced by indomethacin in the rat gastric mucosal surface epithelial cells was studied using a scanning electron microscope. Indomethacin (10 or 25 mg/kg, p.o.) induced a widespread exfoliation of the surface epithelial cells and an exposure of the lamina propria both in the corpus and antrum within 1 hr after the administration.Pretreatment with dmPGE2 (0.3, 3 or 30 acg/kg , p.o.) 30 min before indomethacin (25 mg/kg) dose-dependently inhibited these damages.The effects of dmPGE2, at least on the surface epithelial cells in the corpus, appear to be related to the prevention of damage formation itself and is unrelated to the enhancement of reconstitution of once damaged mucosa. Enhanced gastric motility by indomethacin was potently inhibited by pretreatment with 3 and 30 ug/kg of dmPGE2, but not with 0.3 ug/kg. dmPGE2 pretreatment (30 /cg/kg) significantly decreased the absorption of indomethacin (25 mg/kg) when determined 10 min after giving indomethacin, but did not affect it when determined 30 and 60 min later. We conclude that dmPGE2 protects gastric mucosal surface epithelial cells from indomethacin injury at an early stage, partly by inhibiting gastric motility.

Effects of 16,16-dimethyl prostaglandin E2 on surface epithelial cell damage in the rat stomach induced by vagal nerve stimulation.

“…The damage mainly consisted of a widespread exfoliation of the SEC and exposure of the lamina propria. These features resemble those observed after intragastric application of 50 or 100% ethanol (1, 11), aspirin (1) and indomethacin (2,12). Cho et al (8) reported the development of macroscopically visible damage of the gastric mucosa after VS (2 or 5 V, 20 Hz, 2 msec, 2 hr).…”

“…However, we found that dmPGE2, even at non-antisecretory doses, significantly pro tected the SEC from aspirin and indome thacin-induced damage (1,2). These results indicate that the effects of dmPGE2 on SEC damage induced by various agents, which may be a prerequisite for further development of gastric mucosal lesions, are different and inconsistent.…”

NSAIDs counteractH. pyloriVacA toxin-induced cell vacuolation in MKN 28 gastric mucosal cells

“…In fact, one 50-mg tablet of Indo or one 500-mg tablet of ASA in ϳ50 ml of water give a final instilled concentration of 2.8 and 55 mM, respectively. Moreover, the concentrations of NSAIDs used in vivo in experimental animals range in different studies from 1.7 to 17 mM for Indo (33,54), from 11 to 130 mM for ASA (17,56), and from 1.9 to 19 mM for NS-398 (24,54). The in vivo relevance of our in vitro study depends on the ability of NSAIDs to permeate the mucus layer lining the mucosal surface of the stomach.…”

Acetaminophen Directly Protects Human Gastric Epithelial Cell Monolayers against Damage Induced by Sodium Taurocholate

“…Some if not all of the cells in our preparation are most likely mucous neck cells as these are the mucous cells which divide and multiply. Secondly, more recent studies have demonstrated partial protection of gastric surface epithelial cells by prosta glandins and mild irritants respectively against damage by indomethacin [36] and ethanol [37] in vivo. Furthermore, Fukuda et al [38] have shown protection of isolated rat gastric-surface epithelial cells by PGE2 against ethanol-induced damage in vitro.…”