Kurokawa T, Joh T, Ikai M, Seno K, Yokoyama Y, Itoh M
1st Department of Internal Medicine, Nagoya City University Medical School, Nagoya, Japan.
Dig Dis Sci. 1998 Sep;43(9 Suppl):113S-117S.
Rebamipide, a novel antiulcer agent, has been shown to protect against gastric injury by free radicals. The effect of rebamipide was examined using two rat models of mucosal injury: the stomach was exposed to luminal perfusion of 10 mM H2O2 for 10 min or to local ischemia for 30 min. The effect of deferoxamine, a chelator of Fe3+, was also evaluated to determine whether Fe3+-mediated production of hydroxyl radicals contributed to the damage induced by H2O2. The pylorus was ligated and a double-lumen cannula was inserted into the forestomach for luminal perfusion. [51Cr]EDTA was administered intravenously and mucosal integrity was monitored by measuring blood-to-lumen [51Cr]EDTA clearance. Rebamipide reduced the increase in EDTA clearance induced by ischemia or H2O2. Furthermore, deferoxamine attenuated the H2O2-induced increase. These results suggest that rebamipide has a protective effect against oxygen radical-mediated gastric damage and that Fe3+ is involved in the H2O2-induced injury.
瑞巴派特是一种新型抗溃疡药物,已被证明可通过清除自由基来保护胃免受损伤。使用两种黏膜损伤大鼠模型研究了瑞巴派特的作用:将胃暴露于10 mM过氧化氢腔内灌注10分钟或局部缺血30分钟。还评估了铁离子螯合剂去铁胺的作用,以确定铁离子介导的羟自由基生成是否导致过氧化氢引起的损伤。结扎幽门并将双腔插管插入前胃进行腔内灌注。静脉注射[51Cr]乙二胺四乙酸,并通过测量血-腔[51Cr]乙二胺四乙酸清除率来监测黏膜完整性。瑞巴派特减少了缺血或过氧化氢诱导的乙二胺四乙酸清除率增加。此外,去铁胺减弱了过氧化氢诱导的增加。这些结果表明,瑞巴派特对氧自由基介导的胃损伤具有保护作用,并且铁离子参与了过氧化氢诱导的损伤。