Mechanism of the antiulcerative action of prostaglandin E2 in the rat's stomach

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A5μg/kg, p.o, dose of prostaglandin E2 (PGE2) was given to male Donryu rats (each weighing about 180g) prior to water immersion. As compared with the untreated control, PGE2 markedly decreased the incidence of water immersion-induced ulcers. This study suggested that PGE2 might stabilize the activities of glandular kallikrein, tissue plasminogen activator and endogenous prostaglandin E. PGE2 was furthermore shown to increase the production of acid mucopolysaccharides (AMPS), especially a total of heparan sulfate (HS), and chondroitin sulfate A, B and C (CS-A, -B, and -C) . Then, the effect of HS, CS-A, CS-B and CS-C on arachidonic acid, collgen and thrombin-induced platelet aggregation in the presence of antithrombin III (AT-III) was investigated by using human platelet-rich plasma. Although arachidonic acid and collagen-induced platelet aggregation was not inhibited by any of these AMPS fractions, only thrombin-induced platelet aggregation was inhibited by the heparin-like effect of HS, CS-A and CS-B. The effect of PGE2 (5μg/kg, p.o.) given prior to the intra-arterial administration of dl-norepinephrine (1μg/kg) was also investigated using Donryu rats. Biomicroscopy showed that PGE2 effectively protected the gastric mucosa against dl-norepinephrine-induced stress, widening the caliber of capillaries and keeping a constant rate of blood flow.
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