Study On The Cellular Immunity Of Danggui Buxue Decoction In Patients With Primary Biliary Cholangitis With Poor Response To Ursodeoxycholic Acid

Primary biliary cholangitis(PBC),also known as primary biliary cirrhosis,is an autoimmune liver disease characterized by cholestasis.Biliary epithelial cells are both target cells that are subject to immune destruction and play an immunomodulatory role in the development of PBC.Ursodeoxycholic acid(UDCA)is the first choice,but about 30%of patients still have poor response to UDCA.Traditional Chinese medicine is still in a state of contending for research on this disease.This topic reviews the progress of PBC research in China and abroad in recent years,and carried out research on the immune mechanism of Danggui Buxue Tang on PBC cells with poor response to UDCA.Objective:To investigate the effect of Danggui Buxue Tang(DBT)on the migration,proliferation and apoptosis of human intrahepatic biliary epithelial cells(HiBEC),and to further discuss the effect of CCN1 protein on immune-mediated bile duct injury.Methods:HiBEC was used as cell model.High-speed centrifugation method was used to prepare DBT.The effect of DBT on HiBEC migration ability was tested by scratch test.CCK-8 method was used to detect the effect of DBT on HiBEC proliferation.Flow cytometry was used to detect the effect of DBT on HiBEC apoptosis.LDH release method was used to detect the effect of DBT on CD8+ T-cell mediated HiBEC injury in peripheral blood of PBC patients.qRT-PCR was used to detect the regulatory effect of DBT on the relative expression of CCN1 protein in HiBEC.Results:With the intervention of DBT,compared with the blank control group,the cell migration and proliferation ability of the experimental group was enhanced(P<0.05),and the apoptosis rate was decreased(P<0.05).The cytotoxicity of CD8H+T-cell to HiBEC in the peripheral blood of PBC patients was reduced(P<0.01),and the relative expression of CCN1 protein in HiBEC was increased(P<0.01).Conclusion:DBT can promote HiBEC proliferation and migration and reduce apoptosis by regulating the expression of CCN1 protein,so as to alleviate immune-mediated bile duct injury.