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Endogenous Prostaglandins (endogenous + prostaglandin)

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Medical Sciences	100%

Selected Abstracts

Effects of prostaglandins on form deprivation myopia in the chick

ACTA OPHTHALMOLOGICA, Issue 5 2000
Niyun Jin
ABSTRACT. Purpose: To investigate the possible role of endogenous prostaglandins in the development of form deprivation myopia, as well as the effects of exogenous prostaglandins using atropine as a positive control. Methods: Monocular form deprivation was accomplished by mounting a translucent occluder on one eye of 2,3 day old chicks for 1,4 weeks. Ocular occlusion for 1,2 weeks was used for pharmacological blocking experiments. The axial length of the eye was measured by ultrasonography. Results: Indomethacin, administered intramuscularly, subconjunctivally or intra-vitreally had no significant effect on myopia development. Exogenous PGE2, PGF2, and latanoprost acid administered subconjunctivally, or topically as isopropyl ester eyedrops had no statistically significant effect on the myopia development. However, PGF2, significantly (p<0.01) attenuated the development of myopia after intravitreal injection. The other two prostaglandins had no statistically significant effect. Conclusions: Endogenous prostaglandins are unlikely to play a significant role in the development of form deprivation myopia in the chick. However, PGF2, suprisingly seems to retard the development of form deprivation myopia, but only when administered intravitreally. Whether the mechanism of the myopia retardation is direct or indirect remains unknown. [source]

Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000
K. Takeuchi
Summary Background: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or NG -nitro- l -arginine methyl ester (L-NAME). Results: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. Conclusions: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine. [source]

Gastroprotective activity of ferruginol in mice and rats: effects on gastric secretion, endogenous prostaglandins and non-protein sulfhydryls

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 2 2008
Carlos Areche
The gastroprotective mechanism of the natural diterpene ferruginol was assessed in mice and rats. The involvement of gastric prostaglandins (PGE2), reduced glutathione, nitric oxide or capsaicin receptors was evaluated in mice either treated or untreated with indometacin, N-ethylmaleimide (NEM), N-nitro-L-arginine methyl ester (L-NAME) or ruthenium red, respectively, and then orally treated with ferruginol or vehicle. Gastric lesions were induced by oral administration of ethanol. The effects of ferruginol on the parameters of gastric secretion were assessed in pylorus-ligated rats. Gastric PGE2 content was determined in rats treated with ferruginol and/or indometacin. The reduction of gastric glutathione (GSH) content was determined in rats treated with ethanol after oral administration of ferruginol, lansoprazole or vehicle. Finally, the acute oral toxicity was assessed in mice. Indometacin reversed the gastroprotective effect of ferruginol (25 mg kg,1) but not NEM, ruthenium red or L-NAME. The diterpene (25 mg kg,1) increased the gastric juice volume and its pH value, and reduced the titrable acidity but was devoid of effect on the gastric mucus content. Ferruginol (25, 50 mg kg,1) increased gastric PGE2 content in a dose-dependent manner and prevented the reduction in GSH observed due to ethanol-induced gastric lesions in rats. Single oral doses up to 3 g kg,1 ferruginol did not elicit mortality or acute toxic effects in mice. Our results showed that ferruginol acted as a gastroprotective agent stimulating the gastric PGE2 synthesis, reducing the gastric acid output and improving the antioxidant capacity of the gastric mucosa by maintaining the GSH levels. [source]