Dembiński Artur, Warzecha Zygmunt, Ceranowicz Piotr, Dembiński Marcin, Cieszkowski Jakub, Gosiewski Tomasz, Bulanda Małgorzata, Kuśnierz-Cabala Beata, Gałązka Krystyna, Konturek Peter Christopher
Department of Physiology, Faculty of Medicine, Jagiellonian University Medical College, 16 Grzegórzecka Street, 31-531 Cracow, Poland.
The Second Department of General Surgery, Faculty of Medicine, Jagiellonian University Medical College, 21 Kopernika Street, 31-501 Cracow, Poland.
Gastroenterol Res Pract. 2016;2016:3126280. doi: 10.1155/2016/3126280. Epub 2016 Jun 28.
Background. Inflammatory bowel disease results from the dysregulation of immune response to environmental and microbial agents in genetically susceptible individuals. The aim of the present study was to examine the effect of rifaximin and/or Mutaflor (Escherichia coli Nissle 1917, EcN) administration on the healing of acetic acid-induced colitis. Methods. Colitis was induced in male Wistar rats by rectal enema with 3.5% acetic acid solution. Rifaximin (50 mg/kg/dose) and/or Mutaflor (10(9) CFU/dose) were given intragastrically once a day. The severity of colitis was assessed at the 8th day after induction of inflammation. Results. Treatment with rifaximin significantly accelerated the healing of colonic damage. This effect was associated with significant reversion of the acetic acid-evoked decrease in mucosal blood flow and DNA synthesis. Moreover, administration of rifaximin significantly reduced concentration of proinflammatory TNF-α and activity of myeloperoxidase in colonic mucosa. Mutaflor given alone was without significant effect on activity of colitis. In contrast, Mutaflor given in combination with rifaximin significantly enhanced therapeutic effect of rifaximin. Moreover, Mutaflor led to settle of the colon by EcN and this effect was augmented by pretreatment with rifaximin. Conclusion. Rifaximin and Mutaflor exhibit synergic anti-inflammatory and therapeutic effect in acetic acid-induced colitis in rats.
背景。炎症性肠病是由基因易感个体对环境和微生物因子的免疫反应失调所致。本研究旨在探讨利福昔明和/或米雅(大肠杆菌Nissle 1917,EcN)给药对乙酸诱导的结肠炎愈合的影响。方法。用3.5%乙酸溶液直肠灌肠诱导雄性Wistar大鼠患结肠炎。利福昔明(50mg/kg/剂量)和/或米雅(10⁹CFU/剂量)每天经胃内给药一次。在炎症诱导后第8天评估结肠炎的严重程度。结果。利福昔明治疗显著加速了结肠损伤的愈合。这种作用与乙酸引起的黏膜血流和DNA合成减少的显著逆转有关。此外,利福昔明给药显著降低了结肠黏膜中促炎细胞因子TNF-α的浓度和髓过氧化物酶的活性。单独给予米雅对结肠炎活动无显著影响。相反,米雅与利福昔明联合给药显著增强了利福昔明的治疗效果。此外,米雅导致EcN在结肠定植,且利福昔明预处理增强了这种作用。结论。利福昔明和米雅在大鼠乙酸诱导的结肠炎中表现出协同抗炎和治疗作用。