熊胆粉及熊去氧胆酸调控免疫性血小板减少症模型小鼠Ly6Chigh单核细胞迁移的机制研究OA

Objective:To observe the effect of Bear bile and UDCA on circulating blood Ly6Chigh monocyte chemotaxis receptor CCR2 and its ligand CCL2(MCP-1)in model mice with Immune Thrombocytopenia(ITP),and explore the possible mechanism of regulating Ly6Chigh monocyte migration and reference studies on bear bile and its replacements in ITP management.Methods:Following established methods,an ITP model was induced via immunization in 50 BALB/c mice,randomLy allocated into five groups:normal control,model control,prednisone treatment,bear bile treatment,and UDCA treatment,from the 6th day of making model,mice in the each group was administered 0.4 mL/d volume of corresponding drug by irrigation treatment.From the 6 h,7th day,15th day,automatic blood cytometer was used to dynamic detect platelet count.after treatment 10 day,Flow cytometry was used to detect the changes of the Ly6Chigh monocyte in circulating blood,Enzyme-linked immunosorbent Assay was used to detect the levels of serum MCP-1(monocyte chemotactic protein-1).Results:After the 6 hour of making model,the counts of platelet decreased obviously in all group,reaching the lowest point on the 7th day,and remained at a relatively low level until the 15th day.There was a statistically significant difference compared to the normal group(P<0.05).After treatment,the platelet counts of bear bile,prednisone and UDCA group increased obviously(P<0.01).Flow cytometry results showed that compared with the model group,the positive rate of circulating Ly6Chigh monocytes and its surface chemokine receptor CCR2 in bear bile,UDCA and prednesone groups decreased(P<0.01,P<0.001),while CX3CR1 expression increased(P<0.001).Enzyme-linked immunosorbent Assay results showed that compared with the model group,the levels of MCP-1 in bear bile,UDCA and prednesone groups decreased(P<0.001).Conclusion:The Bear bile and UDCA can downregulate the expression of CCR2 by reducing the level of MCP-1 in circulating blood,thus governs CCL2-CCR2 mediated Ly6Chigh monocyte emigration,reduce the Ly6Chigh monocytes in the circulating blood,this represents a crucial mechanism driving Ly6Chigh monocyte accumulation during ITP progression and worsening.