EFFECT OF Helicobacter pylori infection Normalization in phospholipids concentration of the gastric mucosa after eradication of in patients with peptic ulcer.

幽门螺杆菌感染对消化性溃疡患者根除后胃粘膜磷脂浓度正常化的影响。

• 批准号: 10670487
• 负责人: IWAKIRI Ryuichi
• 金额: $ 1.73万
• 依托单位: Saga Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670487/
• 关键词: Helicobacter pylori; Apoptosis; Phospholipids; Gastric ulcer; Duodenal ulcer; phosphatidylcholine; 胃癌; スナネズミ

Phospholipids in the gastric mucosa form a hydrophobic layer in the epithelium, contributing to the mucosal protective system. Previous study showed that phospholipids concentration in the gastric mucosa decreased in the patients of Helicobacter pylori (H.pylori) infection and that the decrease was, in part, due to lipolytic activity of phopholipase A2 and phopholipase C, which H.pylori produced. In contrast, we previously demonstrated that phospholipids concentration decreased in patients with gastric and/or duodenal ulcer regardless of H.pylori infection. The aim of this study was to examine an effect of eradication of H.pylori on mucosal phospholipids in peptic ulcer. Methods : The endoscopic biopsy specimens were obtained form the antral and corporal mucosa of patients with peptic ulcer : gastric ulcer, n=26 ; duodenal ulcer, n=13 ; agematched H.pylori negative control, n=20. Eradication was performed by lansoprazole 30 mg b.d., amoxycillin 500 mg t.d., clarithromaycin 400 mg b.d., … More and polaprezinc 150 mg b.d. for seven days. Three months after the eradication, the endoscopic biopsy specimens obtained. Phospholipids (phosphatidylcholine : PC, phosphatidyl ethanolamine : PE, and sphingonomyeline : SM) were measured quantitatively in the lipid extract from the biopsy specimens according to thin-layer chromatography and flame ionization detection method. Results : Regarding gastric ulcer, 25 out of 26 patients were eradicated H.pylori, and 12 out of 13 duodenal ulcer patients were eradicated. Compared to the H.pylori negative control group, contents of PC and PE decreased significantly in the gastric ulcer group in both antral and corporal mucosa. This decrease returned to the control level after the eradication. In the duodenal ulcer group, the decrease in the mucosal content of PC and PE was observed only in the antral mucosa, but not in the corporal mucosa. The decrease in the antral mucosal phospholipids in the duodenal ulcer group was returned to the control level after the eradication of H.pylori. The mucosal content of SM did not differ in the three tested groups.Conclusion : This study demonstrated that the eradication of H.pylori in patients with gastric or duodenal ulcer normalized the decrease in PC and PE in the gastric mucosa. The eradication could lessen the deterioration of the protective system of the gastric mucosa, which might be a reason for prevention of recurrence in peptic ulcer after the eradication. Less

胃粘膜中的磷脂在上皮中形成疏水层，有助于粘膜保护系统。先前的研究表明，幽门螺杆菌（H.pylori）感染患者胃粘膜中的磷脂浓度降低，这种降低部分是由于H.pylori产生的磷脂酶A2和磷脂酶C的脂解活性。与此相反，我们以前证明，无论幽门螺杆菌感染的胃和/或十二指肠溃疡患者的磷脂浓度下降。本研究的目的是检查幽门螺杆菌根除对消化性溃疡粘膜磷脂的影响。研究方法：内镜活检标本取自消化性溃疡患者的胃窦和胃体粘膜：胃溃疡，n=26 ;十二指肠溃疡，n=13 ;年龄匹配的幽门螺杆菌阴性对照，n=20。兰索拉唑30 mg b.d.进行根除，阿莫西林500 mg t.d.，克拉霉素400 mg b.d.， ...更多信息 和泊普瑞锌150 mg b.d.七天。根除后3个月，取内镜活检标本。磷脂（磷脂酰胆碱：PC，磷脂酰乙醇胺：PE，和鞘氨醇：SM）定量测定的脂质提取物从活检标本根据薄层色谱法和火焰离子化检测方法。结果：26例胃溃疡患者中有25例根除了幽门螺杆菌，13例十二指肠溃疡患者中有12例根除了幽门螺杆菌。与H.pylori阴性对照组相比，胃溃疡组胃窦和胃体粘膜PC和PE含量均显著降低。根除后，这种下降恢复到对照水平。在十二指肠溃疡组中，仅在胃窦粘膜中观察到粘膜PC和PE含量的减少，而在胃体粘膜中未观察到。幽门螺杆菌根除后，十二指肠溃疡组胃窦粘膜磷脂的减少恢复到对照水平。SM的粘膜内容没有显着差异，在三个测试groups.Conclusion：这项研究表明，根除幽门螺杆菌在胃或十二指肠溃疡患者正常PC和PE在胃粘膜中的减少。胃黏膜保护系统的破坏可能是预防消化性溃疡根除后复发的原因之一。少

项目成果

Yoshida T, Iwakiri R, Noda T, Okamoto K, Kojima M, Fukuyama K, Fujimoto K.: "Histaminergic effect on apoptosis of rat small intestinal mucosa after ischemia-reperfusion."Dig Dis Sci.. 45 (6). 1138-44 (2000)

Yoshida T、Iwakiri R、Noda T、Okamoto K、Kojima M、Fukuyama K、Fujimoto K.：“组胺能对缺血再灌注后大鼠小肠粘膜细胞凋亡的影响。”Dig Dis Sci.. 45 (6)。

Kashiwagi Y, Fujimoto K, Iwakiri R, Yoshida T, Noda T, Aw TY, Niho Y, Sakata T.: "Loss of diurnal variation in ornithine decarboxylase and apoptosis in small intestine of Mongolian gerbils."J Gastroenterol.. 35 (6). 434-40 (2000)

Kashiwagi Y、Fujimoto K、Iwakiri R、Yoshida T、Noda T、Aw TY、Niho Y、Sakata T.：“蒙古沙鼠小肠中鸟氨酸脱羧酶的昼夜变化和细胞凋亡。”J Gastroenterol.. 35（6

Iwakiri R, et al.: "Programmed cell death in rat intestine : effect of feeding and fasting."Scand.J.Gastroenterol.. 36・1. 39-47 (2001)

Iwakiri R 等人：“大鼠肠道中的程序性细胞死亡：进食和禁食的影响”。Scand.J.Gastroenterol.. 36・1 (2001)。

Iwakiri R, et al.: "Endoscopic injection sclerotherapy for esophageal varices prolonged survival of patients with hepatocellular carcinoma complicating liver cirrhosis"Gastrointest.Endosc.. 51・5. 569-572 (2000)

Iwakiri R等人：“食管静脉曲张的内窥镜注射硬化疗法延长了肝硬化合并肝细胞癌患者的生存”Gastrointest.Endosc.. 51・5（2000）。

Noda T, Iwakiri R, Fujimoto K, Yoshida T, Utsumi H, Sakata H, Hisatomi A, Aw TY.: "Suppression of apoptosis is responsible for increased thickness of intestinal mucosa in streptozotocin-induced diabetic rats."Metabolism. 50 (3). 259-264 (2001)

Noda T、Iwakiri R、Fujimoto K、Yoshida T、Utsumi H、Sakata H、Hisatomi A、Aw TY.：“细胞凋亡的抑制是链脲佐菌素诱导的糖尿病大鼠肠粘膜厚度增加的原因。”代谢。