南方医科大学学报 ›› 2004, Vol. 24 ›› Issue (12): 1353-1358.

• • 上一篇    下一篇

姜黄素对模型大鼠肠粘膜炎症因子的调控

简燕婷1, 王继德1, 麦国丰2, 张亚历1, 赖卓胜1   

  1. 1. 南方医科大学南方医院消化研究所, 广东, 广州, 510515;
    2. 江门市卫生局江门市红十字会诊疗所, 广东, 江门, 529000
  • 出版日期:2004-12-20 发布日期:2004-12-20
  • 基金资助:
    收稿日期:2004-5-19。
    基金项目:国家自然科学基金(30270078);广东省中医药基金(1040191);
    作者简介:简燕婷(1967- ),女,副教授,1990年毕业于广州医学院,现为南方医科大学南方医院消化内科博士研究生,电话:020-61641544,E-mail:jyt821_jyt821@yahoo.com.cn.
    通讯作者:张亚历,男,教授,博士研究生导师,E-mail:zhangyl@fimmu.com

Modulation of intestinal mucosal inflammatory factors by curcumin in rats with colitis

JIAN Yan-ting1, WANG Ji-de1, MAI Guo-feng2, ZHANG Ya-li1, LAI Zhuo-sheng1   

  1. 1. 南方医科大学南方医院消化研究所, 广东, 广州, 510515;
    2. 江门市卫生局江门市红十字会诊疗所, 广东, 江门, 529000
  • Online:2004-12-20 Published:2004-12-20

摘要: 目的 炎症性肠病(inflam matory bowel disease,IBD)肠道粘膜炎症与转录因子核因子-κappaB(NF-κB)密切相关。该研究探索NF-κB抑制剂姜黄素IBD动物模型大鼠大肠粘膜炎症因子调控的机制。筛选IBD的靶向治疗药物。方法 建立以5%三硝基苯磺酸(5%TNBS)诱导的肠炎大鼠模型,肠炎的大鼠给予含2.0%的姜黄素饲料,药物阳性对照组给予含0.5%柳氮磺胺吡啶(SASP)的饲料,模型组及阴性对照组给予普通饲料。评价病理组织学评分的变化。应用半定量RT-PCR检测炎症因子mRNA的表达。结果 姜黄素改善肠炎模型大鼠病理组织学症象。姜黄素可显著抑制肠炎模型大鼠肠粘膜致炎因子IL-1βmRNA的高表达,同时可显著提高抗炎因子IL10mRNA的低表达,抗炎因子IL-4mRNA在各组均未见表达。结论 研究显示,NF-κB抑制剂姜黄素可调控IBD鼠科模型中的炎症因子IL-1βmRNA和IL-10mRNA表达。姜黄素有可能是一种有潜能的IBD的靶向药物。

Abstract: Objective To explore the mechanism of modulation of intestinal mucosal inflammatory factors by curcumin, the inhibitor of the transcriptional factor nuclear factor -κB (NF-κB), in rats with trinitrobenzene sulfonic acid (TNBS)-induced colitis, and screen for a targeted therapeutic agent for treatment of inflammatory bowel disease (IBD). Methods Rats with TNBS-induced colitis were fed with diet containing 2.0% curcumin (treatment group), 0.5% sulfasalazine (SASP, positive control group), and normal diet (model group and negative control group). Changes in colonic mucosal histological scores were evaluated and the cytokine mRNA expressions in the colonic tissue assessed by semiquantitative reverse transcriptional PCR (RT-PCR). Results Treatment with curcumin ameliorated the histopathologic signs in rats with TNBS-induced intestinal inflammation. Curcumin and sulfasalazine obviously suppressed the high expression of proinfiammatory cytokine interleukin (IL)-1β mRNA and increased the low expression of IL-10 mRNA in the colonic mucosa. Expression of the anti-inflammatory cytokine IL-4 mRNA was detected in none of the groups. Conclusions Curcumin could modulate the expressions of IL-1β and IL-10 mRNA in murine model of IBD, which suggests the potential of curcumin as a targeted therapeutic agent for IBD.

中图分类号: