Qingjie Fuzheng Granule Treats Ulcerative Colitis Via Regulating Th17/treg Cells Balance

Objective:To observe the anti-inflammatory effect of Qingjie Fuzheng Granules(QFG)on ulcerative colitis(UC)induced by DSS in vivo experiments,and to reveal the mechanism of QFG relieving UC from the perspective of Th17/Treg cell balance,which laid the experimental foundation for the clinical application of QFG in the treatment of UC.Methods:1.The UC mouse model was established by DSS induction,and the mice were administrated with QFG(1 g/kg)and normal saline by gavage.The animals were sampled and analyzed on the 15 th day.2.General growth,weight change,fecal occult blood and disease activity index(DAI)of mice were observed and colon length was recorded.3.HE staining was used to observe the pathological injury of colon tissue.4.The expression levels of TGF-β,IFN-γ and IDO1 in serum of mice were detected by ELISA.5.The serum levels of relative cytokines were determined by Bio-Plex.6.The relative gene m RNA expressions in spleen and colon tissues of mice were detected by RT-q PCR.7.The expressions of RORγt and Foxp3 in spleen and colon were detected by Western Blot.8.The expressions of RORγt and Foxp3 in spleen and IDO1 in colon were observed by IHC.Results:1.QFG could improve the pathological condition of UC mice induced by DSS.2.QFG could significantly inhibit the shortening of colon length in UC mice,improve the pathological changes of colon tissue,and decrease the expression of IL-1β,TNF-α,IFN-γ,IL-6 cytokines and IDO1 expression.3.QFG significantly decreased the expression of Th17-related cytokines(IL-17,IL-21,IL-22,IL-25)and increased the expression of Treg-related cytokines(IL-10,TGF-β).The expression of transcription factor RORγt was decreased in Th17 cells of UC mice,and the expression of transcription factor Foxp3 was increased in Treg cells.Conclusion:QFG can inhibit inflammation in DSS induced UC mice,and can inhibit Th17 cell differentiation,promote Treg cell differentiation,and maintain Th17/Treg cell balance by regulating the expression of transcription factors RORγt and Foxp3.