溃结灵对溃疡性结肠炎大鼠Th17分化的调节机制研究

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目的:探讨溃结灵对溃疡性结肠炎(UC)大鼠Th17细胞分化相关因子的影响,从而揭示其作用机制。方法:采用雄性SD大鼠制作由三硝基苯磺酸(TNBS)所导致的溃疡性结肠炎模型,溃结灵高、中、低剂量以及柳氮磺胺吡啶(SASP)对溃疡性结肠炎大鼠给予治疗,治疗结束后采集结肠粘膜,采用酶联免疫吸附(ELISA)法检测大鼠结肠粘膜中白细胞介素6(IL-6)、转化生长因子β1(TGF-β1)的含量;采用荧光定量PCR检测大鼠结肠组织IL-6、TGF-β1、孤独核受体t(RORγt)、信号转导子与转录激活子3(STAT3)mRNA的表达;采用Western blot法检测结肠粘膜RORγt、STAT3蛋白表达。结果:溃结灵高剂量(18.3g/kg)和中剂量(9.2g/kg)可明显减少溃疡性结肠炎大鼠结肠的溃疡个数和溃疡面积。大鼠结肠粘膜中,模型组IL-6的含量及mRNA表达明显高于正常组,溃结灵高剂量组(18.3g/kg)和柳氮磺胺吡啶组(0.5g/kg)低于模型组;模型组TGF-β1的含量及mRNA表达明显低于正常组,溃结灵高剂量(18.3g/kg)和柳氮磺胺吡啶组(0.5g/kg)高于模型组。模型组结肠粘膜中RORγt、STAT3蛋白表达及mRNA表达明显高于正常组,溃结灵高(18.3g/kg)、低(4.6g/kg)剂组和柳氮磺胺吡啶组(0.5g/kg)的蛋白表达及mRNA表达低于模型组。结论:溃结灵可能通过调节溃疡性结肠炎大鼠结肠粘膜内与Th17分化相关的IL-6、TGF-β1、RORγt、STAT3的表达,从而抑制炎症反应,治疗溃疡性结肠炎。 Objective: To investigate the effect of Kuijieling on Th17 cell differentiation-related factors in ulcerative colitis (UC) rats, and to reveal its mechanism of action. Methods: A model of ulcerative colitis induced by trinitrobenzene sulfonic acid (TNBS) was made in male Sprague-Dawley rats. The ulcerative colitis was induced by ulcer colitis with high, medium and low doses of cusp, and sulfasalazine (SASP) The rats were given treatment. Colonic mucosa was collected after treatment. The contents of IL-6 and TGF-β1 in colonic mucosa of rats were detected by enzyme linked immunosorbent assay (ELISA) The expression of IL-6, TGF-β1, RORγt, signal transducer and activator of transcription 3 (STAT3) mRNA in the colon tissues of rats were detected by quantitative PCR. The expressions of RORγt, STAT3 Protein. Results: Kuijilingling high dose (18.3g / kg) and medium dose (9.2g / kg) can significantly reduce the ulcer colitis ulcerative colitis and ulcer area. In the colonic mucosa of rats, the content and mRNA expression of IL-6 in the model group were significantly higher than those in the normal group. The high-dose Jiegu Ling group (18.3g / kg) and the sulfasalazine group (0.5g / kg) . The content of TGF-β1 and the mRNA expression of TGF-β1 in model group were significantly lower than those in normal group. The high-dose Kuijilingling (18.3g / kg) and sulfasalazine group (0.5g / kg) The expression of RORγt, STAT3 protein and mRNA in colonic mucosa in model group were significantly higher than those in normal group (P <0.05) ) Protein expression and mRNA expression was lower than the model group. Conclusion: Kuijieling can inhibit the inflammatory reaction and treat ulcerative colitis by regulating the expression of IL-6, TGF-β1, RORγt and STAT3 in the colonic mucosa of ulcerative colitis rats.
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