Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) appears to play a critical role in modulating gastric mucosal defense. Administration of NO donors has been reported to protect the gastrointestinal mucosa against damage induced by several irritants. However, the possible role of NO in healing existing ulcers must be clarified further. Therefore, the present study was designed to assess the effect of modulation of NO on the healing of an indomethacin-induced peptic ulcer using a NO precursor, L-arginine, and a competitive inhibitor of NO synthase, L-NAME. Results of administering L-arginine were compared to those using nitroglycerin (NTG), an NO donor. Rats were injected with a single oral dose of indomethacin (30 mg/kg) and then treated with L-arginine (200 mg/kg, i.p.), NTG (1 mg/kg, i.p.) or L-NAME (15 mg/kg, i.p.) once daily for 7 d starting 4 h after the indomethacin injection. Gross lesion examination and histological assessment were done. NO, prostaglandin (PGE2), and mucin content in gastric tissue were detected. In addition, oxidative stress markers including glutathione (GSH) and lipid peroxides were measured. L-arginine and NTG almost completely healed indomethacin-induced ulceration as indicated by macroscopic and histological examination, restoration of normal levels of NO and GSH, and a significant attenuation of the increase in PGE2 and lipid peroxides induced by indomethacin. In contrast, L-NAME was found to exacerbate mucosal damage. In conclusion, the present study provides further evidence for the role of NO in gastric ulcer healing and it suggests an alternative path to treating the universal problem of non-steroidal anti-inflammatory-drug-induced gastropathy.
 ...
PMID:The potential therapeutic effect of nitric oxide modulators in experimentally-induced gastric ulcers. 2249 Dec 10

Background Epidemiological studies have suggested an association between Helicobacter pylori (H pylori) infection and atherosclerosis through undefined mechanisms. Endothelial dysfunction is critical to the development of atherosclerosis and related cardiovascular diseases. The present study was designed to test the hypothesis that H pylori infection impaires endothelial function through exosome-mediated mechanisms. Methods and Results Young male and female patients (18-35 years old) with and without H pylori infection were recruited to minimize the chance of potential risk factors for endothelial dysfunction for the study. Endothelium-dependent flow-mediated vasodilatation of the brachial artery was evaluated in the patients and control subjects. Mouse infection models with CagA+ H pylori from a gastric ulcer patient were created to determine if H pylori infection-induced endothelial dysfunction could be reproduced in animal models. H pylori infection significantly decreased endothelium-dependent flow-mediated vasodilatation in young patients and significantly attenuated acetylcholine-induced endothelium-dependent aortic relaxation without change in nitroglycerin-induced endothelium-independent vascular relaxation in mice. H pylori eradication significantly improved endothelium-dependent vasodilation in both patients and mice with H pylori infection. Exosomes from conditioned media of human gastric epithelial cells cultured with CagA+ H pylori or serum exosomes from patients and mice with H pylori infection significantly decreased endothelial functions with decreased migration, tube formation, and proliferation in vitro. Inhibition of exosome secretion with GW4869 effectively preserved endothelial function in mice with H pylori infection. Conclusions H pylori infection impaired endothelial function in patients and mice through exosome-medicated mechanisms. The findings indicated that H pylori infection might be a novel risk factor for cardiovascular diseases.
 ...
PMID:Helicobacter pylori Infection Impairs Endothelial Function Through an Exosome-Mediated Mechanism. 3217 33