细胞因子在大鼠溃疡性结肠炎模型中的表达研究

The expression of cytokines in experimental ulcerative colitis rat

目的:探讨促炎细胞因子IL-6、TNF-α与抑炎细胞因子IL-10在三硝基苯磺酸(TNBS)/乙醇所致的溃疡性结肠炎(ulcerative colitis,UC)大鼠模型结肠组织中的表达,探讨其在该模型中的作用及意义。方法:雌性SD大鼠随机分为正常对照组及模型组,每组7只。正常对照组不造模,模型组用三硝基苯磺酸(TNBS)/乙醇溶液灌肠复制UC模型。观察两组实验大鼠体质量变化、大体及组织病理学改变,采用酶联免疫吸附法检测细胞因子(IL-6、IL-10、TNF-α)的含量。结果:与正常组比较,模型组大鼠结肠大体形态评分、组织学评分明显升高(0.00±0.00与5.43±1.27,1.29±0.49与6.71±0.95,P<0.01);与正常组比较,模型组大鼠结肠组织IL-6、TNF-α表达明显升高(102.13±7.12与188.27±11.65,87.39±6.74与121.51±8.56,P<0.01);IL-10表达明显下降(202.97±12.26与71.40±8.28,P<0.01)。结论:促炎细胞因子IL-6、TNF-α与抑炎细胞因子IL-10的失衡在TNBS诱导的大鼠UC发病中起重要作用。

Objective To study the expression of proinflammatory cytokines （IL- 6, TNF-α） and anti -inflammatory cytokine （IL- 10） in the colonic tissue of ulcerative colitis rat induced by 2,4,6 -trinitrobenzenesulfonic acid （TNBS） / ethanol and to explore its effect and significance on pathogenesis of TNBS - induced ulcerative colitis （UC）. Method Fourteen female SD rats were randomized into the normal control group and the model group （7 rats in each group）. UC in the model group was induced by intrarectal administration of TNBS （100mg/kg in 50% ethanol）. All animals were killed on day 15. The bodyweight loss of each rat,macroscopical and histological changes of the colon were observed. IL- 6 ,IL- 10 and TNF-α in colonic tissues were tested by ELISA. Results Compared with the normal control group, the macroscopic damage score and histological score of the model group were significantly increased [ （ 0. 00 ± 0. 00） Vs （ 5.43 ± 1.27 ）, （ 1.29 ± 0.49 ） Vs （6.71 ± 0. 95 ）, P 〈 0. 01 ]. Compared with the normal control group, the expression of IL - 6 and TNF - α in the colonic tissues of the model group were significantly increased [ （ 102. 13 ± 7. 12） vs （ 188.27 ± 11.65）, （87.39 ± 6.74） vs （ 121.51 ± 8.56） ,P 〈0. 01 ] ;IL - 10 expression was significantly decreased [ （202. 97 ± 12.26） vs （71.40 ±8. 28） ,P 〈0. 01 ]. Conclusion The imbalance between proinflammatory cytokines （IL- 6 ,TNF- α） and proinfiammatory cytokines （IL -10） plays an important role in the pathogenesis of rats with TNBS - induced ulcerative colitis.