| 摘要: |
| 目的 探讨Toll样受体4(TLR4)、NF-κB p65及负性调控因子Tollip在三硝基苯磺酸(TNBS)诱导的结肠炎大鼠肠黏膜中的表达。方法 40只健康雄性SD大鼠随机分为正常对照组和模型组。采用免疫组织化学及RT-PCR方法 比较两组大鼠肠黏膜TLR4、NF-κB p65和Tollip的表达。结果 TLR4、NF-κB p65 mRNA在模型组肠黏膜中的表达高于正常对照组(TLR4: 0.376±0.029 vs 0.215±0.049, t=2.731, P=0.013； NF-κB p65: 0.746±0.049 vs 0.206±0.063, t=6.055, P=0.000),与大体形态损伤评分(TLR4: r=0.754, P=0.000; NF-κB p65: r=0.548, P=0.012)及组织学损伤评分(TLR4: r=0.866, P=0.000; NF-κB p65: r=0.919, P=0.000)呈正相关。Tollip mRNA在模型组及正常组中表达差异无统计学意义(0.288±0.050 vs 0.140±0.046, t=1.993, P=0.061)；Tollip蛋白在模型组肠黏膜固有层的表达高于正常组；Tollip的表达与大体形态损伤评分(r=-0.497, P=0.026)及组织学损伤评分(r=-0.551，P=0.012)呈负相关。结论 Toll 样受体4与负性调控因子Tollip的表达失衡参与了炎症性肠病的发病机制。 |
| 关键词: Toll样受体4 NF-κB p65 Tollip 结肠炎 肠黏膜 |
| DOI：10.3724/SP.J.1008.2012.032 |
| 投稿时间：2011-11-05修订日期：2011-12-15 |
| 基金项目:山东省自然科学基金(ZR2009CL006). |
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| Expression of Toll-like receptor 4 and its negative regulating factor Tollip in colonic mucosa of rats with experimental colitis |
| XU Ning1△,YU Zhen-hai2,3△*,WANG Zhi-qiang2,QU Hong-lin2,SUN Yi2,LIU Jiao2 |
(1. Department of Gastroenterology, Affiliated Yantai Yuhuangding Hospital, Qingdao University Medical School, Yantai 264000, Shandong, China
2. Department of Human Anatomy, Binzhou Medical University, Binzhou 256603, Shandong, China
3. Department of Human Anatomy, College of Basic Medical Sciences, Second Military Medical University, Shanghai 200433, China
△Co-first authors.
*Corresponding author.) |
| Abstract: |
| Objective To investigate the expression of Toll-like receptor 4 (TLR4), NF-κB p65 and the negative regulating factor Toll-interacting protein (Tollip) in colonic mucosa of rats with 2，4，6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis. MethodsForty healthy male SD rats were randomly divided into normal control group and model group. The expression of TLR4, NF-κBp65 and Tollip was detected and compared between the two groups by immunohistochemistry(IHC) and RT-PCR. ResultsRT-PCR revealed a significant higher expression of TLR4 and NF-κB p65 mRNA in the model group compared with the normal control group (TLR4: 0.376±0.029 vs 0.215±0.049, t= 2.731, P=0.013； NF-κB p65: 0.746±0.049 vs 0.206±0.063, t=6.055, P=0.000). The expression of TLR4 and NF-κB p65 was positively correlated with the general injury score (TLR4: r=0.754, P=0.000; NF-κB p65: r=0.548, P=0.012) and the histological injury score (TLR4: r=0.866, P=0.000; NF-κB p65: r=0.919, P=0.000). Expression of Tollip mRNA was not significantly different between the two groups as detected by RT-PCR (0.288±0.050 vs 0.140±0.046, t=1.993, P=0.061). IHC revealed that Tollip protein expression was mainly assembled in the colonic mucosal lamina propria, and the expression in the model group was higher than that in the normal control group. Tollip expression was negatively correlated with the general injury score (r=-0.497, P=0.026) and the histological injury score (r=-0.551，P=0.012). ConclusionThe unbalanced expression of TLR4 and the negative regulating factor Tollip participates in the pathogenesis of inflammatory bowel disease. |
| Key words: Toll-like receptor 4 NF-κB p65 Tollip colitis intestinal mucosa |
