Wakabayashi H, Orihara T, Nakaya A, Miyamoto A, Watanabe A
Third Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
J Gastroenterol Hepatol. 1998 Jun;13(6):566-71. doi: 10.1111/j.1440-1746.1998.tb00691.x.
To investigate the effect of Helicobacter pylori infection on the 'gastric mucosal barrier', phospholipid contents and the fatty acid composition of endoscopic biopsy specimens of the gastric mucosa were analysed in healthy volunteers with and without H. pylori infection. The gastric corporeal phosphatidylcholine (PC) content of H. pylori-positive healthy volunteers was less than that of H. pylori-negative healthy volunteers (P < 0.05). Moreover, H. pylori-positive healthy volunteers had a decrease in linoleic acid composition (P < 0.0001) and an increase in arachidonic acid composition (P < 0.0001) and in the arachidonic acid/linoleic acid ratio (P < 0.0001) of antral and corporeal PC compared with H. pylori-negative healthy volunteers. These findings suggest that H. pylori infection enhances production of various eicosanoids, resulting in changes in the gastric mucosal phospholipid contents and their fatty acid composition, that may consequently cause the gastric mucosal barrier to be weakened.
为研究幽门螺杆菌感染对“胃黏膜屏障”的影响，对有和没有幽门螺杆菌感染的健康志愿者的胃黏膜内镜活检标本的磷脂含量和脂肪酸组成进行了分析。幽门螺杆菌阳性健康志愿者的胃体磷脂酰胆碱（PC）含量低于幽门螺杆菌阴性健康志愿者（P<0.05）。此外，与幽门螺杆菌阴性健康志愿者相比，幽门螺杆菌阳性健康志愿者胃窦和胃体PC的亚油酸组成降低（P<0.0001），花生四烯酸组成增加（P<0.0001），花生四烯酸/亚油酸比值增加（P<0.0001）。这些发现表明，幽门螺杆菌感染会增强各种类花生酸的产生，导致胃黏膜磷脂含量及其脂肪酸组成发生变化，进而可能导致胃黏膜屏障减弱。
