Ogino K, Hobara T, Ishiyama H, Yamasaki K, Kobayashi H, Izumi Y, Oka S
Department of Public Health, Yamaguchi University, School of Medicine, Ube, Japan.
Eur J Pharmacol. 1992 Feb 25;212(1):9-13. doi: 10.1016/0014-2999(92)90065-c.
The mechanism of the inhibitory action of rebamipide, a new mucosal protective drug, was studied using rats with diethyldithiocarbamate-induced gastric antral ulcers. Rebamipide reduced ulcer formation and inhibited the elevation in lipid peroxide concentration in the gastric mucosa. Rebamipide inhibited both luminol- and lucigenin-dependent chemiluminescence of neutrophils activated by formyl-methionyl-leucyl-phenylalanine. Rebamipide did not alter the reduction of cytochrome c induced by the xanthine-xanthine oxidase system or the NADPH-dependent microsomal lipid peroxidation in the liver. These findings suggest that rebamipide prevents diethyldithiocarbamate-induced gastric ulcer formation by inhibiting neutrophil activation.
使用二乙基二硫代氨基甲酸盐诱导胃窦溃疡的大鼠,研究了新型黏膜保护药物瑞巴派特的抑制作用机制。瑞巴派特减少了溃疡形成,并抑制了胃黏膜中脂质过氧化物浓度的升高。瑞巴派特抑制了由甲酰甲硫氨酰亮氨酰苯丙氨酸激活的中性粒细胞的鲁米诺和光泽精依赖性化学发光。瑞巴派特并未改变黄嘌呤-黄嘌呤氧化酶系统诱导的细胞色素c还原或肝脏中NADPH依赖性微粒体脂质过氧化。这些发现表明,瑞巴派特通过抑制中性粒细胞激活来预防二乙基二硫代氨基甲酸盐诱导的胃溃疡形成。