Igarashi M, Takagi A, Jiang X, Hasumi K, Watanabe S, Deguchi R, Miwa T
Division of Gastroenterology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Aliment Pharmacol Ther. 2002 Apr;16 Suppl 2:235-9. doi: 10.1046/j.1365-2036.16.s2.6.x.
Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are important factors in gastric mucosal injury. However, the relationship between H. pylori and NSAID-related gastroduodenal mucosal injury has not been clarified.
To determine the role of H. pylori in NSAID-induced gastric mucosal injury and to examine the effects of H. pylori, indomethacin and sofalcone on gastric epithelial cells in culture, as a useful model to study gastric mucosal injury. In addition, we studied the effect of sofalcone, a gastric mucosal protection agent, on H. pylori and NSAID-induced gastric mucosal injury.
Cytotoxic and noncytotoxic strains of H. pylori were used, each with an inoculum of 10(7) cfu/mL. The effect on the growth of RGM-1 cells (a rat gastric epithelial cell line) was studied by MTT assay, and levels of prostaglandin E2 in culture supernatants were measured by EIA.
Both cytotoxic and noncytotoxic strains of H. pylori tended to induce cell injury in RGM-1 cells at 48 h after inoculation. Indomethacin alone induced gastric epithelial injury in a dose-dependent manner, but did not augment cell injury induced by H. pylori. In addition, sofalcone (10(-5) mol/L) showed a suppressive effect on indomethacin-induced gastric epithelial injury.
These findings indicate that indomethacin induces gastric mucosal injury regardless of H. pylori infection, and suggests that sofalcone may be a useful drug in the treatment of NSAID-induced mucosal injury.
幽门螺杆菌和非甾体抗炎药（NSAIDs）是胃黏膜损伤的重要因素。然而，幽门螺杆菌与NSAID相关的胃十二指肠黏膜损伤之间的关系尚未阐明。
确定幽门螺杆菌在NSAID诱导的胃黏膜损伤中的作用，并研究幽门螺杆菌、吲哚美辛和索法酮对培养的胃上皮细胞的影响，作为研究胃黏膜损伤的有用模型。此外，我们研究了胃黏膜保护剂索法酮对幽门螺杆菌和NSAID诱导的胃黏膜损伤的作用。
使用幽门螺杆菌的细胞毒性和非细胞毒性菌株，每种接种物浓度为10(7) cfu/mL。通过MTT法研究对RGM-1细胞（大鼠胃上皮细胞系）生长的影响，并通过酶免疫分析（EIA）测量培养上清液中前列腺素E2的水平。
接种后48小时，幽门螺杆菌的细胞毒性和非细胞毒性菌株均倾向于诱导RGM-1细胞损伤。单独使用吲哚美辛以剂量依赖性方式诱导胃上皮损伤，但并未增强幽门螺杆菌诱导的细胞损伤。此外，索法酮（10(-5) mol/L）对吲哚美辛诱导的胃上皮损伤显示出抑制作用。
这些发现表明，无论是否感染幽门螺杆菌，吲哚美辛都会诱导胃黏膜损伤，并提示索法酮可能是治疗NSAID诱导的黏膜损伤的有效药物。
