ArticleScientific reports2017
Nitric oxide donor protects against acetic acid-induced gastric ulcer in rats via S-nitrosylation of TRPV1 on vagus nerve.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 21 citations in OpenAlex.
- Gastroprotective Effect of Artemisia herba-alba Leaf Extract in Acetic Acid-Induced Gastric Ulceration in Wistar Rats.Chemistry & biodiversity · 2026Article
- Unravelling Peptic Ulcers: Comprehensive Insights into Etiology, Diagnosis, Screening Techniques, and Treatment.Current pharmaceutical design · 2025Review
- Regulation of Ion Channel Function by Gas Molecules.Advances in experimental medicine and biology · 2021Review
- The Relationship Between Protein S-Nitrosylation and Human Diseases: A Review.Neurochemical research · 2020Review
- The role of hydrogen sulfide in gastric mucosal damage.Medical gas researchReview
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was conducted to investigate the effects of nitric oxide (NO) in acetic acid-induced gastric ulcer of rats and the underlying mechanisms. We found that peritoneal injection of sodium nitroprusside (SNP), a NO donor, decreased the ulcer area, inflammatory cell infiltration and MPO degree in acetic acid-induced gastric ulcer in rats. This effect was abolished by a transient receptor potential vanilloid 1 (TRPV1) antagonist or prior subdiaphragmatic vagotomy. SNP increased the jejunal mesenteric afferent discharge in a dose-depended manner, which was largely diminished by pretreatment of S-nitrosylation blocker N-ethylmaleimide, TRPV1 antagonist capsazepine, genetic deletion of TRPV1, or vagotomy. Whole-cell patch clamp recording showed that SNP depolarized the resting membrane potential of NG neurons, and enhanced capsaicin-induced inward current, which were both blocked by N-ethylmaleimide. Our results suggest that NO donor SNP alleviates acetic acid-induced gastric ulcer in rats via vagus nerve, while S-nitrosylation of TRPV1 may participate in this route. Our findings reveal a new mechanism for vagal afferent activation, and a new potential anti-inflammatory target.
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