复方青黛颗粒对溃疡性结肠炎模型大鼠结肠组织TGF-β1和VEGF表达影响

Effect of Compound Qingdai Granula on the expression of TGF-β1 and VEGF in the colon tissue of rats with ulcerative colitis

[目的]观察复方青黛颗粒对溃疡性结肠炎(UC)大鼠结肠组织转化生长因子-β1(TGF-β1)与血管内皮生长因子(VEGF)表达的影响,进一步探讨复方青黛颗粒治疗UC的相关机制。[方法]三硝基苯磺酸(TNBS)法制备大鼠UC模型,随机分为空白对照组、模型对照组、柳氮磺吡啶(SASP)组及复方青黛颗粒低、中、高剂量组。治疗结束后取大鼠结肠组织,用RT-PCR方法检测TGF-β1及VEGF mRNA表达。[结果]与空白对照组比较,模型对照组TGF-β1及VEGF基因表达明显增高(P<0.05),复方青黛颗粒高剂量组TGF-β1基因表达较模型对照组显著下降(P<0.05),VEGF基因表达较模型对照组显著升高(P<0.05)。[结论]复方青黛颗粒对TNBS诱导的UC大鼠的治疗作用可能与下调TGF-β1过度表达及上调VEGF有关。

[Objective]To explore the effect of Compound Qingdai Granula（CQO） on the expression of transforming growth factor betal（TOF-β1）and vascular endothelial growth factor（VEOF）in colon tissues of rats with ulceratire colitis（UC）, and to investigate the related mechanism of CQG in treating UC. [Methods] The rat model of UC was induced by trinitrobenzene sulfonic acid （TNBS） and then divided into control group,model group, salazosulfapyridine （SASP） group,low-dose CQG group （CQG-L）, moderatedose CQG group（CQCr-M）, and high-dose CQG group（CQG-H）. Except the control group, the other groups were given intragastrically normal saline, SASP, and different concentrations of CQG respectively from day 3 after model establishment for 10 days. On day 14, the rats were killed. The colon tissue and serum of the rats were taken for detection of TGF-β1 and VEGF expression using reverse transcription-polymerase chain reaction （RT-PCR）[Results] The gene expression of TGF-β1 and VEGF in the model group were significantly higher than that in the control group（P〈0. 05）. The gene expression of TGF-β1 of the CQG-H group was significantly lower than that in the model group, while VEGF expression of the CQG-H group was significantly higher than that in the model group. [Conclusion]The expression of colonic TGF- β1 and VEGF were markedly decreased on the fourteenth day after the administration of CQG. Therefore,it can be speculated that the therapeutic effect of CQG on UC induced by TNBS in rats may be correlated with down regulating over-expression of TGF-β1 and up-regulating VEGF expression.