Effects of 16, 16-Dimethyl-Prostaglandin E2 on Ammonia- and Ethanol-Induced Mucosal Lesions in the Rat

Murakami, Motonobu; Yoo, Jung Keun; Saita, Hiroshi; Seiki, Masao; Inada, Masami; Miyake, Teruki

doi:10.1097/00004836-198812001-00011

Cited by 9 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This protective effect of plasmin inhibitors was not affected by the pretreatment with indomethacin, suggesting that the protection is independent of the action of endogenous prostaglandins. We previously reported that exogenous 16,16 dmPGE2 had a protective effect against ethanol-induced gastric lesions, but not against ammonia-induced lesions in rats (9). In contrast, the present study clearly demon strated that plasmin inhibitor markedly pro tected the gastric mucosa against both ammonia and ethanol.…”

contrasting

confidence: 82%

Cytoprotective effect of plasmin inhibitor on necrotizing agent-induced gastric lesions in rats.

et al. 1989

Self Cite

View full text Add to dashboard Cite

contrasting

confidence: 82%

Cytoprotective effect of plasmin inhibitor on necrotizing agent-induced gastric lesions in rats.

et al. 1989

Self Cite

View full text Add to dashboard Cite

“…Previous studies showed that the occurrence of gastrointestinal hemorrhage lesions increased 1 h after administration of ethanol (Szabo et al, 1985; Murakami et al, 1988). In this study, both macroscopic and histological evaluations of gastric lesions showed that ethanol-induced gastric hemorrhage lesions and damage to gastric mucosa in rats were reduced after treatment with GF and GFC versus the M group.…”

Section: Discussionmentioning

confidence: 99%

Treatment Mechanism of Gardeniae Fructus and Its Carbonized Product Against Ethanol-Induced Gastric Lesions in Rats

Zhang

Wang

et al. 2019

Front. Pharmacol.

View full text Add to dashboard Cite

Gardeniae Fructus (GF) and carbonized GF (GFC) have been shown to exert a gastrointestinal protective effect and are frequently used in clinical practice for the treatment of hemorrhage and brown stool. In this study, we employed a combination of pharmacological methods and metabolomics in a rat model of ethanol-induced acute stomach ulcer to investigate the gastroprotective effect of GF and GFC water extracts and the potential mechanism involved in this process. The levels of nitric oxide (NO) and interleukin 6 (IL-6) in the plasma of rats were determined. The results showed that both GF and GFC reduced the ethanol-induced gastric lesions and expression of NO and IL-6 in these rats. Of note, 16 and 11 feature metabolites were filtered and identified in the GF and GFC groups, respectively. Both GF and GFC act by restoring the biosynthesis of valine, leucine, and isoleucine, and the metabolism of glycerophospholipids. Moreover, histological evaluation revealed that heat processing of GF to create GFC enhanced the gastric mucosa protective effect. Furthermore, heat processing converted the main pathway from alanine, aspartate, and glutamate metabolism, associated with GF, to histidine metabolism, associated with GFC. GF and GFC ameliorated gastric mucosa lesions in rats via reductions in NO production and inflammatory cytokine secretion, and the induction of prostaglandin E2.

show abstract

“…However, dmPGE 2 was ten times less potent in ammonia-induced cell damage than in ethanol-induced damage. Murakami et al [48] reported that dmPGE 2 afforded less protection against ammonia-induced gastric mucosal lesions than against ethanol-induced lesions. Although it remains unknown why the cell protection against ammonia is less than that against ethanol, our in vitro study may provide the explanation for the little gastroprotection afforded by dmPGE 2 against ammonia-induced mucosal lesions.…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective Mechanism of Lafutidine, a Novel Anti-ulcer Drug with Histamine H2-Receptor Antagonistic Activity

Onodera¹,

Shibata²,

Tanaka³

et al. 2011

Arzneimittelforschung

View full text Add to dashboard Cite

Lafutidine (CAS 118288-08-7, FRG-8813) is a novel histamine H2-receptor antagonist with gastroprotective activity. The aim of this study was to investigate the property of the gastro-protective activity of lafutidine by examining the effect on ammonia-induced change in transmucosal potential difference (PD), basal gastric mucosal blood flow (GMBF) and noxious agent-induced cell damage. Intragastrical application of lafutidine accelerated the recovery of the PD reduction after exposure of the mucosa to 0.25% ammonia solution and the accelerating effect was abolished by chemical deafferentation, but not with indometacin, a cyclooxygenase inhibitor. The application of capsaicin, as a reference compound, significantly promoted the recovery of the ammonia-induced PD reduction and this effect was not altered with indometacin. Lafutidine given intragastrically caused a sustained increase in GMBF in a dose-dependent fashion, which was also completely inhibited in the deafferentated rats. In vitro studies revealed that, in contrast to 16,16-dimethyl prostaglandin E2, lafutidine did not protect isolated gastric superficial epithelial cells from ethanol- or ammonia-induced damage. In conclusion, the gastroprotection of lafutidine is induced by promoting the restitution of the damaged mucosa after a noxious agent, not by directly protecting the epithelial cells and this effect may be caused through the mechanism of capsaicin-sensitive afferent nerves.

show abstract

Effects of 16, 16-Dimethyl-Prostaglandin E2 on Ammonia- and Ethanol-Induced Mucosal Lesions in the Rat

Cited by 9 publications

References 0 publications

Cytoprotective effect of plasmin inhibitor on necrotizing agent-induced gastric lesions in rats.

Cytoprotective effect of plasmin inhibitor on necrotizing agent-induced gastric lesions in rats.

Treatment Mechanism of Gardeniae Fructus and Its Carbonized Product Against Ethanol-Induced Gastric Lesions in Rats

Gastroprotective Mechanism of Lafutidine, a Novel Anti-ulcer Drug with Histamine H2-Receptor Antagonistic Activity

Contact Info

Product

Resources

About