Nesfatin-1在伴或不伴幽门螺杆菌感染的相关胃病中的表达

Expression of Nesfatin-1 in patients with gastropathy complicated with or without Helicobacter pylori infection

目的观察Nesfatin-1在不同胃病(慢性胃炎、消化性溃疡)中的表达,尤其是在合并幽门螺杆菌(Helicobacter pylori,Hp)感染与非感染者的胃病患者血清及胃黏膜组织中的差异。方法收集在南京医科大学第一附属医院内镜中心空腹>10 h并同时行胃镜及13C呼气试验患者共50例,采用ELISA法检测患者血清Nesfatin-1水平,同时取胃黏膜组织行逆转录-聚合酶链反应(RT-PCR)检测Nesfatin-1 mRNA,免疫组化检测Nesfatin-l/NUCB2的分布情况。结果 Hp(-)组患者的血清及胃黏膜组织中Nesfatin-1表达明显高于Hp(+)组患者;Hp(+)组中消化性溃疡患者血清及胃黏膜组织中Nesfatin-1表达明显低于非溃疡组。结论 Nesfatin-1表达与Hp感染相关,两者可能共同参与胃酸分泌调节。Nesfatin-1高表达可能对胃内Hp有抑制作用,从而可能影响胃十二指肠疾病的发生。

Objective To investigate the plasma or gastricmucosa levels of Nesfatin-1 in the patients with benign gastropathy,and to elucidate the association between Helicobacter pylori（ Hp） colonization and expression of Nesfatin-1 in human. Methods Fifty adult patients in Endoscopy Center of the First Affiliated Hospital of Nanjing Medical University,who underwent both the upper gastrointestinal endoscopy and13 C breath test were randomly enrolled. Blood samples were collected after a 10 hours fast before endoscopy and biopsies were endoscopically taken from the antrum. The plasma levels of Nesfatin-1 and gastric mucosa expression levels of Nesfatin-1 mRNA were detected by enzyme-linked immune-sorbent assay（ ELISA） and real-time polymerase chain reaction（ RT-PCR）,respectively. The distribution of Nesfatin-1 was examined with immunohistochemical（ IHC） staining. Results The plasma and gastric mucosa levels of Nesfatin-1 were both significantly higher in Hp-negative patients than those in Hp-positive patients. Meanwhile,among those patients with Hp infection,the level of Nesfatin-1 was significantly lower in patients with duodenal ulcer and gastric ulcer than those without ulcers. Conclusions There may be an association between Hp infection and expression of Nesfatin-1 in human. They may jointly play an important role in the regulation of gastric acid secretion. It is suggested that high-level expression of Nesfatin-1 may partly inhibit the colonization of Hp in stomach and then involve in the pathogenesis of gastroduodenal disease.