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Rebamipide promotes healing of colonic ulceration through enhanced epithelial restitution.

机译:瑞巴派特通过增强上皮恢复来促进结肠溃疡的愈合。

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AIM: To investigate the efficacy of rebamipide in a rat model of colitis and restitution of intestinal epithelial cells in vitro. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
机译:目的:研究瑞巴派特在大鼠结肠炎模型中的作用以及体外肠上皮细胞恢复的作用。方法:三硝基苯磺酸(TNBS)在雄性Wistar大鼠中诱发急性结肠炎。从第7天开始,每天接受直肠内瑞巴派特治疗的大鼠,在TNBS给药后第14天处死大鼠。切除远端结肠以评估炎症的各种参数。此外,使用伤口愈合测定法确定用瑞巴派特治疗的大鼠肠上皮(RIE)细胞的恢复性增强。结果:瑞巴派特的结肠内给药可加速TNBS诱导的溃疡愈合。瑞巴派特显着抑制了TNBS给药后结肠湿重的增加。伤口测定显示瑞巴派特通过细胞外信号调节激酶(ERK)的磷酸化和Rho激酶的活化增强了RIE细胞的迁移。结论:瑞巴派特灌肠通过增强ERK活化来增强RIE细胞的复原,从而治愈了肠道损伤。瑞巴派特可能是炎症性肠病的一种新型治疗方法。

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