Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine 602-8566 Kyoto, Japan.
World J Gastroenterol. 2011 Sep 7;17(33):3802-9. doi: 10.3748/wjg.v17.i33.3802.
To investigate the efficacy of rebamipide in a rat model of colitis and restitution of intestinal epithelial cells in vitro.
Acute colitis was induced with trinitrobenzene sulfonic acid (TNBS) in male Wistar rats. Rats received intrarectal rebamipide treatment daily starting on day 7 and were sacrificed on day 14 after TNBS administration. The distal colon was removed to evaluate the various parameters of inflammation. Moreover, wound healing assays were used to determine the enhanced restitution of rat intestinal epithelial (RIE) cells treated with rebamipide.
Intracolonic administration of rebamipide accelerated TNBS-induced ulcer healing. Increases in the wet weight of the colon after TNBS administration were significantly inhibited by rebamipide. The wound assay revealed that rebamipide enhanced the migration of RIE cells through phosphorylation of extracellular signal-regulated kinase (ERK) and activation of Rho kinase.
Rebamipide enema healed intestinal injury by enhancing restitution of RIE cells, via ERK activation. Rebamipide might be a novel therapeutic approach for inflammatory bowel disease.
研究瑞巴派特在结肠炎大鼠模型中的疗效及其对体外肠上皮细胞修复的作用。
采用三硝基苯磺酸(TNBS)诱导雄性 Wistar 大鼠急性结肠炎。从第 7 天开始,大鼠接受直肠内瑞巴派特治疗,在 TNBS 给药后第 14 天处死。切除远端结肠以评估炎症的各种参数。此外,还进行了伤口愈合试验,以确定瑞巴派特处理的大鼠肠上皮(RIE)细胞的修复作用增强。
直肠内给予瑞巴派特可加速 TNBS 诱导的溃疡愈合。瑞巴派特显著抑制 TNBS 给药后结肠湿重的增加。伤口试验表明,瑞巴派特通过细胞外信号调节激酶(ERK)的磷酸化和 Rho 激酶的激活,增强了 RIE 细胞的迁移。
瑞巴派特灌肠通过激活 ERK 增强 RIE 细胞的修复作用来治愈肠道损伤。瑞巴派特可能是一种治疗炎症性肠病的新方法。