Protective effect of exogenous phospholipid on aspirin-induced gastric mucosal injury

Swarm, Robert A.; Ashley, Stanley W.; Soybel, David I.; Ordway, Frederick S.; Cheung, Laurence Y.

doi:10.1016/0002-9610(87)90200-5

Cited by 50 publications

(17 citation statements)

References 11 publications

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“…This finding is interesting because phospholipids are shown to increase mucosal hydrophobicity [40] and mucus viscosity [41], and thereby reduce back-diffusion of hydrogen ions [42]. It is also shown that administration of exogenous phospholipids may pro-tect the gastric mucosa of animals from damage induced by acid [43,44], bile salts [45], and ethanol [46]. As far as we know, the effect of Al-antacids on human intragastric phospholipid concentration has not previously been examined.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of antacids on gastric juice components in duodenal ulcer patients

Weberg

Berstad

1990

Eur J Clin Investigation

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Abstract. In 10 duodenal ulcer patients gastric juice was aspirated every 10 rnin for 20 min before and 200 min after sham feeding. One antacid tablet or placebo was given 80 min after the sham feeding. Analyses of the aspirates showed that antacids reduced mean hydrogen ion activity and pepsin concentration significantly for 40 and 60 min. respectively, and increased phospholipid concentration for 30 min, compared with placebo. Highest mean pH was 2.52. The percentage of pH readings at or above pH levels of 2.3, and 4 during the 2 h period following antacid administration was 29, 10, and 2'21, respectively. N o significant differences between antacid and placebo were found regarding intragastric concentrations of bile acids and prostaglandin E2. When one antacid tablet was administered 80 min after a real meal, the effect on intragastric pH was similarly weak, but lasted slightly longer.'Acid neutraliration' alone can hardly explain the ulcer-healing eflect of low-dose antacids. Antacidinduced increase in intragastric concentration of phospholipids is a new and potentially important observation.

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Section: Discussionmentioning

confidence: 99%

Acute effects of antacids on gastric juice components in duodenal ulcer patients

Weberg

Berstad

1990

Eur J Clin Investigation

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“…Despite intense interest in the mechanism by which intestinal mucosal integrity is lost and maintained, the etiopathologv of stress and chemically induced gastric and duodenal ulcers is far from clear. The gastric mucosa has a hydrophobic lining which is assumed to have protective functions against luminal acid as well as intrinsic and extrinsic corrosive agents [ 1,2], It has been proposed that the hydrophobicity of the mucosal lining is attributed to a surfactant-like phospholipid monolayer adsorbed to the mucosal surface, which acts as a mucosal barrier and impedes back-diffusion of luminal H+ ion into the muco sal tissue [3], This phospholipid monolayer has been shown to defend gastric mucosa against damage induced by strong acids [4] and other barrier-breaking agents [5,6].…”

Section: Introductionmentioning

confidence: 99%

Effect of Quinacrine, a Phospholipase A<sub>2</sub> Inhibitor on Stress and Chemically Induced Gastroduodenal Ulcers

Moutaery

Tariq²

1997

Digestion

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Quinacrine, a phospholipase A₂ inhibitor, has been studied for its ability to inhibit gastric secretion and to protect the gastric and duodenal mucosa against chemically and stress-induced ulcers. Acid secretion studies were undertaken in pylorus-ligated rats with and without quinacrine treatment. Experimental gastric lesions were induced by water-immersion restraint stress, indomethacin and 80% ethanol in rats; whereas duodenal ulcers were produced by treatment of rats with cysteamine. The level of nonprotein sulfhydryl compounds and gastric wall mucus were also measured in the glandular stomach of the rats following ethanol-induced gastric lesions. The results of this study demonstrate that quinacrine produces a dose-dependent inhibition of gastric acid secretion in rats. Pretreatment with quinacrine significantly attenuated the formation of stress-, indomethacin- and ethanol-induced gastric lesions. Quinacrine also protected intestinal mucosa against cysteamine-induced duodenal ulcers. The antiulcer activity of quinacrine was associated with appreciable inhibition of ethanol-induced depletion of nonprotein sulfhydryls and gastric wall mucus. These findings point towards the mediation of sulfhydryls in quinacrine-induced gastrointestinal cytoprotection. In conclusion, this study demonstrates that quinacrine possesses significant antiulcer and cytoprotective activity against various experimentally induced gastroduodenal lesions. Although the mechanism of action of quinacrine requires further evaluation, the experimental observations derived from this study may have future clinical relevance and therefore deserve to be investigated thoroughly.

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“…In animal studies exogenous phospholipids or phospholipids contained in food have been shown to prevent mucosal damage induced by acids, nonsteroidal anti-inflammatory drugs, or bile salts in the stomach, duodenum, and small intestine (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23). Exogenous PC inhibits inflammation in trinitrobenzene sulfonic acid or acetic acid-induced colitis and is described to be anti-fibrinogenetic (24,25).…”

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confidence: 99%

Anti-inflammatory Effects of Phosphatidylcholine

Treede

Braun

Sparla

et al. 2007

Journal of Biological Chemistry

258

210

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We recently showed that mucus from patients with ulcerative colitis, a chronic inflammatory disorder of the colon, is characterized by a low level of phosphatidylcholine (PC) while clinical studies reveal that therapeutic addition of PC using slow release preparations is beneficial. The positive role of PC in this disease is still elusive. Here we tested the hypothesis that exogenous application of PC has anti-inflammatory properties using three model systems. First, human Caco-2 cells were treated with tumor necrosis factor-␣ (TNF-␣) to induce a pro-inflammatory response via activation of NF-B. Second, latex bead phagosomes were analyzed for their ability to assemble actin in vitro, a process linked to pro-inflammatory signaling and correlating with the growth versus killing of mycobacteria in macrophages. The third system used was the rapid assembly of plasma membrane actin in macrophages in response to sphingosine 1-phosphate. TNF-␣ induced a pro-inflammatory response in Caco-2 cells, including 1) assembly of plasma membrane actin; 2) activation of both MAPKs ERK and p38; 3) transport of NF-B subunits to the nucleus; and 4) subsequent up-regulation of the synthesis of pro-inflammatory gene products. Exogenous addition of most PCs tested significantly inhibited these processes. Other phospholipids like sphingomyelin or phosphatidylethanolamine showed no effects in these assays. PC also inhibited latex bead phagosome actin assembly, the killing of Mycobacterium tuberculosis in macrophages, and the sphingosine 1-phosphate-induced actin assembly in macrophages. TNF-␣ induces the activation of signaling molecules and the reorganization of the actin cytoskeleton in human intestinal cells. Exogenous application of PC blocks pro-inflammatory signaling in Caco-2 cells, in phagosomes in vitro and facilitates intracellular survival of mycobacteria. We provide further evidence that actin assembly by membranes is part of the pro-inflammatory response. Collectively, these results provide a molecular foundation for the clinical studies showing a beneficial effect of PC therapy in ulcerative colitis.

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Protective effect of exogenous phospholipid on aspirin-induced gastric mucosal injury

Cited by 50 publications

References 11 publications

Acute effects of antacids on gastric juice components in duodenal ulcer patients

Acute effects of antacids on gastric juice components in duodenal ulcer patients

Effect of Quinacrine, a Phospholipase A<sub>2</sub> Inhibitor on Stress and Chemically Induced Gastroduodenal Ulcers

Anti-inflammatory Effects of Phosphatidylcholine

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