作者: Ting Han , Yan Tang , Jing Li , Bing Xue , Liping Gong
DOI: 10.1038/S41598-017-02275-1
关键词:
摘要: This study was conducted to investigate the effects of nitric oxide (NO) in acetic acid-induced gastric ulcer rats and underlying mechanisms. We found that peritoneal injection sodium nitroprusside (SNP), a NO donor, decreased area, inflammatory cell infiltration MPO degree rats. effect abolished by transient receptor potential vanilloid 1 (TRPV1) antagonist or prior subdiaphragmatic vagotomy. SNP increased jejunal mesenteric afferent discharge dose-depended manner, which largely diminished pretreatment S-nitrosylation blocker N-ethylmaleimide, TRPV1 capsazepine, genetic deletion TRPV1, Whole-cell patch clamp recording showed depolarized resting membrane NG neurons, enhanced capsaicin-induced inward current, were both blocked N-ethylmaleimide. Our results suggest donor alleviates via vagus nerve, while may participate this route. findings reveal new mechanism for vagal activation, anti-inflammatory target.