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目的:观察清肠化湿方对三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎(UC)小鼠模型Treg细胞的影响,探讨其治疗UC的作用机制和靶点。方法:使用TNBS造模成功后,分为空白组、模型组、清肠化湿方组、柳氮磺胺吡啶(SASP)组。灌胃给药连续7d后,处死小鼠;流式细胞仪检测脾脏中CD4+CD25+Treg细胞Foxp3的表达,免疫组化法观察结肠组织中Foxp3的浸润情况,实时荧光定量PCR法检测特异性转录因子Foxp3 mRNA的基因水平。结果:模型组小鼠脾脏与结肠组织中Foxp3表达均较空白组明显减少(P<0.01),结肠组织中Foxp3 mRNA水平降低(P<0.05);清肠化湿方组小鼠脾脏CD4CD25Treg细胞Foxp3表达以及结肠组织Foxp3 mRNA水平均明显高于模型组(P<0.01,P<0.001),免疫组化观察Foxp3浸润较模型组增多(P<0.05)。结论:清肠化湿方可能通过上调脾脏及结肠组织中Foxp3表达,促进Treg细胞形成,维持免疫耐受,从而发挥抗炎作用。
Objective: To observe the effect of Qingchang Huashi prescription on Treg cells induced by trinitrobenzene sulfonic acid (TNBS) in murine model of ulcerative colitis (UC) and explore its mechanism of action and target. Methods: After successful establishment of TNBS model, the rats were divided into blank group, model group, Qingchang Huashi Decoction group and sulfasalazine (SASP) group. The mice were sacrificed 7 days after gavage administration, the Foxp3 expression in CD4 + CD25 + Treg cells in spleen was detected by flow cytometry, the Foxp3 infiltration in colon tissues was observed by immunohistochemical method, and the specificity was detected by real-time fluorescence quantitative PCR Gene level of transcription factor Foxp3 mRNA. Results: The expression of Foxp3 in spleen and colonic tissue in model group was significantly lower than that in blank group (P <0.01), Foxp3 mRNA in colon tissue was decreased (P <0.05) (P <0.01, P <0.001). Foxp3 infiltration was increased in the model group than in the model group (P <0.05) by immunohistochemistry. Conclusion: Xiaochang Huashi Decoction may exert anti-inflammatory effects by up-regulating Foxp3 expression in spleen and colon, promoting Treg cell formation and maintaining immune tolerance.