The Effects And Significances Of IFNa-2a On Bcl-2 Genes In Hepatic Tissue

Objetive: To study the IFNα-2a on rat liver tissue Bcl-2 gene expression and the mechanism of liver fibrosis.Methods: Hepatic fibrosis was induced in rats by subcutaneous injection of CCl4.SD rats were randomly divided into fibrosis model group(A),control group(B) and IFNα-2a intervention group(C). The samples were collected respectively in four weeks and eight weeks.Automatic biochemical analyzer samples of serum liver function alanine aminotransferase(ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), albumin (ALB), radioimmunoassay detection of liver fibrosis markers hyaluronic acid (HA), laminin (LN), procollagen III (PIII), IV collagen (IVC). Using RT-PCR detection the expression of Bcl-2 of the rats liver in each group,liver tissue samples were detected by the conventional HE, reticular fiber staining and Masson staining.Results: Rat liver fibrosis model was successfully established. Liver function ALT, AST and liver fibrosis markers HA, LN, PIII of IFNα-2a intervention group in four and eight weeks than the fibrosis model group were lower (P<0.01); Liver function ALT,AST,ALB and liver fibrosis markers HA, LN, PIII of fibrosis model group in four weeks than eight weeks were higher (P<0.01). Liver fibrosis and fatty degeneration in IFNα-2a intervention group than fibrosis model group significantly reduced,but the extent of hepatic inflammation was not significantly different.Liver fibrosis model group in eight weeks showed the formation of false lobules.Bcl-2 gene expression of IFNα-2a intervention group, fibrosis model group and control group in four weeks, respectively (1.18±0.01)%,(1.22±0.01)% and (1.15±0.01)%, F = 384.00; Bcl-2 gene expression of IFNα-2a intervention group, fibrosis model group and control group in eight weeks ,respectively (0.96±0.02)%, (0.98±0.03)% and (0.86±0.03)%, F = 191.11. Bcl-2 gene expression of IFNα-2a intervention group was significantly lower than the fibrosis model group (P<0.01); control group was significantly lower than IFNα-2a intervention group and fibrosis model group (P < 0.01).Conclusions: The establishment of CCl4-induced rat liver fibrosis model, the time four weeks better than eight weeks (0.3ml/100g by subcutaneous injection 50% CCl4, twice weekly).IFNα-2a can effectually prevent hepatic fibrosis induced by CCl4 and decrease liver fatty degeneration. The mechanism of preventing hepatic fibrosis and decreasing liver fatty degeneration is related with Bcl-2 gene expression.It may be to control apoptosis of HSC by adjusting the expression of Bcl-2 gene.