期刊文献+

中药清肠栓对溃疡性结肠炎大鼠结肠通透性的影响 被引量:11

Effect of Qingchang Suppository on Intestinal Permeability in Rats with Ulcerative Colitis
下载PDF
导出
摘要 目的探讨复方中药清肠栓对三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎(UC)大鼠结肠黏膜通透性的影响及其修复结肠溃疡的作用机制。方法采用异硫氰酸荧光素-右旋糖4000(FITC-dextran4000,FD-4)作为标记物,在体实验与离体实验相结合测定大鼠结肠通透性,观察中药清肠栓对UC大鼠结肠通透性的影响。结果 (1)在体动物实验:发现模型组大鼠结肠对FD-4的通透性较正常组显著增加,在30min内增加为对照组的6倍。清肠栓高剂量及中剂量组能不同程度的抑制UC大鼠结肠通透性的升高(P<0.05)。(2)离体实验:通过测定FD-4的通透性系数(Papp)反映发现,大鼠升结肠黏膜通透性120min内,模型组FD-4的Papp为(5.001±1.316)×10-8cm/s,Papp增加为正常组的2.5倍,清肠栓高剂量及中剂量组能有效降低升结肠黏膜对FD-4的Papp(P<0.05)。结论清肠栓能有效抑制UC大鼠结肠通透性的升高,改善肠黏膜屏障功能,促进溃疡愈合。 Objective To observe the effect of Qingchang Suppository(QCS,a Chinese herbal preparation)on intestinal permeability in rat ulcerative colitis(UC)model induced by trinitrobenzene sulforic acid,and to explore the mechanism of QCS for healing the ulceration.Methods Labelled by FITC-dextran 4 000(FD-4),the permeability of colonic membrane in UC rat and effect of QCS on it were observed in vitro and in vivo.Results In vivo study showed that the colonic FD-4 permeability of UC rat was increased significantly,being 6-fold of normal in 30 min.After treated with QCS of high/moderate dosage,it significantly attenuated to different degrees(P0.05).FD-4 permeability coefficient(Papp)determination in vitro showed that Papp in model rats increased to(5.001± 1.316)×10-8cm/s in 120 min,being 2.5-fold of control;and which could be decreased by high/moderate dose QCS effectively(P0.05).Conclusion QCS could suppress the high colonic permeability in UC model rats,improve the barrier function of intestinal membrane and promote the healing of ulceration.
作者 卢璐 谢建群
出处 《中国中西医结合杂志》 CAS CSCD 北大核心 2010年第10期1087-1090,共4页 Chinese Journal of Integrated Traditional and Western Medicine
基金 国家自然科学基金资助项目(No.30772801)
关键词 清肠栓 溃疡性结肠炎 肠道通透性 Qingchang Suppository ulcerative colitis intestinal permeability
  • 相关文献

参考文献8

  • 1王皓,欧阳钦,胡仁伟.三硝基苯磺酸结肠炎动物模型的建立[J].胃肠病学,2001,6(1):7-10. 被引量:177
  • 2Xiao DT,Hong C,Xiao WQ,et al.Platelet-activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E-cadherin[J].Br J Pharmacol,2000,129(7):1522-1529.
  • 3Fan Y,Wu DZ,Gong YQ,et al.Effects of calycosin on the impairment of barrier function induced by hypoxia in human umbilical vein endothelial cells[J].Eur J Pharmacol,2003; 481(1):33-40.
  • 4Lewis K,Caldwell J,Phan V,et al.Decreased epithelial barrier function evoked by exposure to metabolic stress and nonpathogenic E.Coli is enhanced by TNF-alpha[J].Am J Physiol Gastrointest Liver Physiol,2008,294(2):G669-G678.
  • 5Bruewer M,Luegering A,Kucharzik T,et al.Proinflammatory cytokins disrupt epithelial barrier function by apoptosis-independent mechanisms[J].J Immunol,2003,171(9):6164-6172.
  • 6Xavier RJ,Podolsky DK.Unravelling the pathogenesis of inflammatory bowel disease[J].Nature,2007,448(1):427-434.
  • 7Ferrier L,Berard F,Debrauwer L,et al.Impairment of the intestinal barrier by ethanol involves enteric microflora and mast cell activation in rodents.Am J Pathol,2006,168(4):1148-1154.
  • 8Wang Q,Fang CH,Hasselgren PO.Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6knockout mice[J].Am J Physiol Regulat Integr Comp Physiol,2001,281(3):R1013-R1023.

二级参考文献7

  • 1Butzner JD, Parmar R, Bell CJ, Dalai V. Butyrateenema therapy stimulates mucosal repair in experimental colitis in the rat. Gut, 1996, 38: 568~573.
  • 2Dieleman LA, Palmen MJ, Akol H, Bloemena E,Pena AS, Meuwissen SG, Van Rees EP. Chronicexperimental colitis induced by dextran sulphatesodium (DSS) is characterized by Th1 and Th2 cy-tokines. Clin Exp Immunol, 1998, 114: 385~391.
  • 3Beagley KW, Black CA, Elson CO. Strain differences in susceptibility to TNBS-induced colitis(abstract). Gastroenterology, 1991, 100: A560.
  • 4Ward M. The pathogenesis of Crohn's disease.Lancet, 1977, 2: 903-905.
  • 5Shorter RG, Huizenga KA, Spencer RJ. A working hypothesis for the etiology and pathogenesisof nonspecific inflammatory bowel disease. Am JDig Dis, 1972, 17: 1024~ 1032.
  • 6Kunin S, Gallily R. Recognition and lysis of altered-self cells by macrophages. I. Modification oftarget cells by 2, 4, 6-trinitrobenzene sulphonicacid. Immunology, 1983, 48: 265~272.
  • 7Grisham MB, Volkmer C, Tso P, Yamada T. Metabolism of trinitrobenzene sulfonic acid by the ratcolon produces reactive oxygen species. Gastroenterology, 1991, 101: 540~547.

共引文献176

同被引文献149

引证文献11

二级引证文献193

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部