痛泻要方对溃疡性结肠炎大鼠结肠黏膜STAT3基因和蛋白表达的影响

Effects of Tongxie Yaofang on the STAT3 mRNA and protein expressions of colonic mucosa in rats with experimental ulcerative colitis

目的:观察痛泻要方对溃疡性结肠炎(UC)模型大鼠血清白介素-6(IL-6)、结肠黏膜STAT3蛋白和基因表达的影响,探讨其作用机制。方法:受试动物随机分为空白组,模型组,痛泻要方高、中、低剂量组及美沙拉秦(5-ASA)组,每组15只,痛泻要方低、中、高剂量组分别按生药1.4、2.8、5.6g/kg剂量灌胃,美沙拉秦组给药剂量为0.5g/kg,通过测定各组大鼠血清IL-6浓度、结肠组织STAT3蛋白和基因水平,探索痛泻要方对UC的干预机制。结果:与空白组比较,模型组大鼠血清IL-6含量、结肠组织STAT3基因和蛋白的表达量均明显升高(P<0.01);治疗后,痛泻要方高剂量组与美沙拉秦组血清IL-6含量、STAT3基因和蛋白的表达量较模型组均明显降低(P<0.05,P<0.01)。结论:痛泻要方对肝郁脾虚型UC大鼠模型血清IL-6含量、结肠黏膜STAT3基因和蛋白的表达有下调作用,提示痛泻要方治疗UC的作用可能与抑制或阻断IL-6/JAK/STAT3信号转导途径有关。

Objective: To observe the effects of Tongxie Yaofang on the serum IL-6 as well as STAT3 m RNA and protein expressions of colonic mucosa in rats with experimental ulcerative colitis(UC), and then identify its underlying mechanism of action. Methods: The rats were randomly divided into control group, model group, Tongxie Yaofang high, medium and low dose groups and Mesalazine(5-ASA) group, with 15 rats in each group. The Tongxie Yaofang low, medium and high dose groups were administered separately with 1.4, 2.8, 5.6g/kg crude drugs, and the dosage for 5-ASA group was 0.5g/kg. Through the determination of serum IL-6 concentration as well as colonic tissue STAT3 protein and gene level, the intervention mechanism of Tongxie Yaofang on UC was explored. Results: Compared with the control group, the concentration of serum IL-6 and the expression level of colonic tissue STAT3 gene and protein in model group rats were significantly increased(P<0.01); after medication, the concentration of serum IL-6 and the expression level of colonic tissue STAT3 gene and protein in both Tongxie Yaofang high dose group and 5-ASA group were evidently lower than those in the model group(P<0.05, P<0.01). Conclusion: Tongxie Yaofang can reduce the concentration of serum IL-6 as well as the expression level of colonic tissue STAT3 gene and protein in UC rats with stagnation of liver qi and spleen deficiency, which suggests that Tongxie Yaofang in the treatment of UC may inhibit or block the IL-6/JAK/STAT3 signal transduction pathway.