Both selective COX-1 and COX-2 inhibitors aggravate gastric damage induced in rats by 2-deoxy-D-glucose. relation to gastric hypermotility and COX-2 expression.

Background/aim: 2-deoxy-D-glucose (2DG), despite causing gastric hypermotility via vagal stimulation, does not by itself induce damage in the stomach but produces gross lesions under prostaglandin (PG) deficiency induced by non-ulcerogenic dose of indomethacin. In this study, we examined the roles PG and cyclo-oxygenase (COX) isozymes play in the gastric ulcerogenic effect of 2DG in the rat stomach under PG deficiency caused by indomethacin.

Methods: The animals were given 2DG i.

Dopamine-induced protection against indomethacin-evoked intestinal lesions in rats--role of anti-intestinal motility mediated by D2 receptors.

Background: Although it is known that dopamine prevents various gastrointestinal lesions, the underlying mechanism remains unclear. In the present study, we examined the protective effect of dopamine on indomethacin-induced small intestinal lesions, in relation to intestinal hypermotility.

Material/methods: Male SD rats received indomethacin (10 mg/kg) subcutaneously (s.

Role of cyclooxygenase (COX)-1 and COX-2 inhibition in nonsteroidal anti-inflammatory drug-induced intestinal damage in rats: relation to various pathogenic events.

We recently reported that cyclooxygenase (COX)-2 expression was up-regulated in the rat small intestine after administration of indomethacin, and this may be a key to nonsteroidal anti-inflammatory drug (NSAID)-induced intestinal damage. In the present study, we investigated the effect of inhibiting COX-1 or COX-2 on various intestinal events occurring in association with NSAID-induced intestinal damage. Rats without fasting were treated with indomethacin, SC-560 (a selective COX-1 inhibitor), rofecoxib (a selective COX-2 inhibitor), or SC-560 plus rofecoxib, and the following parameters were examined in the small intestine: the lesion score, the enterobacterial number, myeloperoxidase (MPO) and inducible nitric-oxide synthase (iNOS) activity, and intestinal motility.

Mechanisms by which endogenous glucocorticoid protects against indomethacin-induced gastric injury in rats.

We investigated the mechanisms underlying the protective action of glucocorticoids against indomethacin-induced gastric lesions. One-week adrenalectomized rats with or without corticosterone replacement (4 mg/kg sc) were administered indomethacin (25 mg/kg sc), and gastric secretion (acid, pepsin, and mucus), motility, microvascular permeability, and blood glucose levels were examined. Indomethacin caused gastric lesions in sham-operated rats, with an increase in gastric motility and microvascular permeability as well as a decrease in mucus secretion.

16,16-Dimethyl prostaglandin E2 inhibits indomethacin-induced small intestinal lesions through EP3 and EP4 receptors.

We evaluated the effect of various PGE analogs specific to EP receptor subtypes on indomethacin-induced small intestinal lesions in rats and investigated the relationship of EP receptor subtype with the PGE action using EP receptor knockout mice. Animals were administered indomethacin subcutaneously, and they were killed 24 hr later. 16,16-dimethyl prostaglandin E2 (dmPGE2) or various EP agonists were administered intravenously 10 min before indomethacin.

Up-regulation of cyclooxygenase-2 by inhibition of cyclooxygenase-1: a key to nonsteroidal anti-inflammatory drug-induced intestinal damage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) induce gastrointestinal ulceration as the adverse reaction. This effect of NSAIDs is attributable to endogenous prostaglandin (PG) deficiency caused by inhibition of cyclooxygenase (COX), yet the relation between COX inhibition and the gastrointestinal ulcerogenic property of NSAIDs remains controversial. Using selective COX inhibitors, we examined whether inhibition of COX-1 or COX-2 alone is sufficient for induction of intestinal damage in rats.

Protective effect of thiaton, an antispasmodic drug, against indomethacin-induced intestinal damage in rats.

The effect of thiaton [3-(di-2-thienylmethylene)-5-methyl-trans-quinolizidinium bromide], an antispasmodic drug, on indomethacin-induced intestinal damage was examined in rats. The animals were given indomethacin, s.c.