期刊文献+

姜黄素对溃疡性结肠炎的作用及机制研究 被引量:9

下载PDF
导出
摘要 目的:研究姜黄素治疗溃疡性结肠炎的作用及其机制。方法:用2,4二硝基氯苯(DNCB)建立大鼠创伤性溃疡结肠炎模型,观察姜黄素对其结肠黏膜组织病理学、结肠损伤分数、红细胞超氧化物歧化酶(SOD)和结肠黏膜过氧化脂质(LPO)的影响。结果:造模大鼠经姜黄素治疗,结肠黏膜光镜下组织学有显著改变,结肠损伤分数、大便乳酸含量降低,红细胞SOD活性升高,肠黏膜LPO含量降低,TLR4、TLR2因子表达进一步减弱,疗效优于阳性对照组(P<0.01)。结论:姜黄素发挥抗溃疡性结肠炎的机制之一可能与其减弱TLR4、TLR2的表达,降低结肠黏膜LPO含量,增加红细胞SOD活性,进而增加机体对O2.-的清除,从而促进大便乳酸排泄,减少结肠炎症损伤有关。
出处 《中药材》 CAS CSCD 北大核心 2013年第2期291-294,共4页 Journal of Chinese Medicinal Materials
基金 2009江西省科技支撑计划项目(2009BSB11201)
  • 相关文献

参考文献14

  • 1NeumanMG. Immune dysfunction in inflammatory bowel disease [J]. Transl Res,2007,149(4) :173-184.
  • 2陈胜,邹开芳,杨天,谭琰,丁炎波,钱伟.Toll样受体(TLR)2、TLR4和TLR9在大鼠结肠炎模型结肠组织中的表达及其意义[J].胃肠病学,2007,12(6):339-343. 被引量:25
  • 3Okayasu I, Hatakeyama S, Yamada M, et al. A novel meth- od in the induction of reliable experimental acute and chro- nic ulcerative colitis in mice [J]. Gastroenterology, 1990, 98:694.
  • 4于树玉.肿瘤宿主全血清中脂质过氧化水平动态变化及抗氧剂对其影响.中华肿瘤杂志,2004,1:5-6.
  • 5Ardizzone S, Porro GB. Biologic therapy for inflammatory bowel disease [ J]. Drugs ,2005,65 (16) :2253-2861.
  • 6Domenech E. Inflammatory bowel disease: Current thera- peutic options [ J]. Digestion ,2006,73 ( 1 ) :672-761.
  • 7Jian Y T, Mai G F, Wang J D, et al. Preventive and thera- peutic effect s of NF2kappaB inhibitor curcumin in rats co- litis-induced by trinit robenzene sulfonic acid [ J]. World J Gastro-entero1,2005,12 ( 11 ) : 1747-1752.
  • 8Holt P R, Katz S, Kirshoff R. Curcumin therapy in inflam- matory bowel disease, a pilot study [ J ]. Dig Dis Sci,2005, 50:2191-2193.
  • 9Fiocchi C. Inflammatory bowel disease:etiology and patho- genesis [ J]. Gastoenterology, 1998,115 : 182-205.
  • 10Sands BE. Therapy of inflammatory bowel disease [ J ]. Gastroenterology,2000,118:568-582.

二级参考文献12

  • 1张政,王福生.CpG-ODN免疫学功能及其应用研究[J].免疫学杂志,2003,19(S1):122-125. 被引量:11
  • 2徐宁,欧阳钦,于振海,李甘地,李希诗,王春晖.Toll样受体4、CD14和核因子-κB在溃疡性结肠炎中的表达及临床意义[J].中华消化杂志,2005,25(7):433-434. 被引量:20
  • 3Hibi T, Ogata H, Sakuraba A. Animal models of inflammatory bowel disease. J Gastroenteml, 2002, 37 (6): 409-417.
  • 4Murano M, Maemura K, Hirata I, et al. Therapeutic effect of intracolonically administered nuclear factor kappa B (p65) antisense oligonucleotide on mouse dextran sulphate sodium (DSS)-induced colitis. Clin Exp Immunol, 2000, 120 (1): 51-58.
  • 5Yoshimura A, Lien E, Ingalls RR, et al. Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2. J Immunol, 1999, 163 (1): 1-5.
  • 6Ulevitch RJ. Toll gates for pathogen selection. Nature, 1999, 401 (6755): 755-756.
  • 7Krieg AM. CpG motifs in bacterial DNA and their immune effects. Annu Rev Immunol, 2002, 20: 709-760.
  • 8Sartor RB. Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colit.is. Nat Clin Pract Gastroenterol Hepatol, 2006, 3 (7): 390-407.
  • 9Cario E, Podolsky DK. Differential alteration in intestinal epithelial cell expression of toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease. Infect Immun, 2000, 68 (12): 7010-7017.
  • 10Hausmann M, Kiessling S, Mestermann S, et al. Toll-like receptors 2 and 4 are up-regulated during intestinal inflammation. Gastroenterology, 2002, 122 (7): 1987-2000.

共引文献26

同被引文献158

引证文献9

二级引证文献93

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