Figure 6.

The prevention and treatment mechanism of FZHY on CCl4-induced hepatic fibrosis through regulating the recruitment and polarization of intrahepatic macrophages. FZHY reduced CCL2 gene expression of proinflammatory Kupffer cells which were activated in CCl4-damaged liver tissue, thereby reducing the recruitment of proinflammatory Ly6C^high macrophages. Meanwhile, FZHY promoted the phenotype polarization of proinflammatory Kupffer cells to anti-inflammatory Kupffer cells and increased CX3CL1 gene expression in intrahepatic macrophages, thereby it promoted the polarization and recruitment of restorative Ly6C^low macrophages. Anti-inflammatory Kupffer cells and restorative Ly6C^low macrophages exerts their anti-inflammation and antiliver fibrosis effects.