Hepatoprotective effects of silybin in liver fibrosis

Table 1 Different phases of inflammatory conditions in liver that progress towards the fibrosis of the liver tissues

Extent of damage	Possible cellular mechanisms
Stage 1: Cell recruitment	Neutrophills and macrophages activation, hence, activation of reticuloendothelial cells
Stage 2: Inflammatory cytokines	Increase in the levels of TNF-α, TGF-β, PGE2, IL-1 along with decrease in the levels of SOD, GSH
Stage 3: Tissue damage	Increase in extracellular matrix production, deposition and degradation along with decrease in Tissue inhibitors of matrix metalloproteinases
Stage 4: Fibrinogenesis	Persistant activation of inflammatory cascade is associated with the destruction or liver parenchyma which eventually leads to fibrosis

PGE₂: Prostaglandin E₂; TNF-α: Tumor necrosis factor α; IL: Interleukin; SOD: Superoxidedismutase; TGF-β: Transforming growth factor-β.