Hayashi S, Sugiyama T, Amano K, Isogai H, Isogai E, Aihara M, Kikuchi M, Asaka M, Yokota K, Oguma K, Fujii N, Hirai Y
Department of Microbiology, Jichi Medical School, Tochigi-ken 329-0498, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan.
Antimicrob Agents Chemother. 1998 Aug;42(8):1895-9. doi: 10.1128/AAC.42.8.1895.
Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H. pylori to human gastric epithelial cells is the initial step of H. pylori infection. Inhibition of H. pylori adhesion is thus a therapeutic target in the prevention of H. pylori infection. Experiments were performed to evaluate the effect of rebamipide, a novel antiulcer agent, on H. pylori adhesion to gastric epithelial cells. MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells. Ten H. pylori strains isolated from patients with chronic gastritis and gastric ulcer were used in the study. We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay. The adhesion of H. pylori to MKN-28 and MKN-45 cells was significantly inhibited by pretreatment of these cells with 100 microg of rebamipide per ml. However, the adhesion was not affected by the pretreatment of H. pylori with rebamipide. On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide. Our studies suggest that rebamipide inhibits the adhesion of H. pylori to gastric epithelial cells.
幽门螺杆菌是胃十二指肠疾病的主要病原体。幽门螺杆菌与人胃上皮细胞的黏附是幽门螺杆菌感染的起始步骤。因此,抑制幽门螺杆菌黏附是预防幽门螺杆菌感染的一个治疗靶点。开展实验以评估新型抗溃疡药物瑞巴派特对幽门螺杆菌黏附胃上皮细胞的影响。源自人胃癌的MKN - 28和MKN - 45细胞用作靶细胞。研究使用了从慢性胃炎和胃溃疡患者中分离出的10株幽门螺杆菌菌株。我们采用先前建立的酶联免疫吸附测定法定量评估瑞巴派特对幽门螺杆菌黏附MKN - 28和MKN - 45细胞的影响。用每毫升100微克瑞巴派特预处理这些细胞后,幽门螺杆菌对MKN - 28和MKN - 45细胞的黏附受到显著抑制。然而,用瑞巴派特预处理幽门螺杆菌并不影响其黏附。另一方面,瑞巴派特不影响幽门螺杆菌、MKN - 28细胞和MKN - 45细胞的活力。我们的研究表明,瑞巴派特可抑制幽门螺杆菌对胃上皮细胞的黏附。