Objective:To research the effect of TNF-α inhibitors on hepatitis C virus（HCV）infection in hepatocytes. Methods:Hepatoma Huh7 cells were cultured in vitro. Huh7 cells divided into four groups:untreated group

NFκB inhibitors [6-amino-4-（4-phenoxyphenylethylamino） quinazoline

QNZ] treated group

caffeic acid phenethyl ester（CAPE）) treated group and TNF-α inhibitors（Lenalidomide）treated group. Concentrations of the inhibitors were from 100 μmol/L to 1.28 nmol/L with 5-fold serial dilution in each group. Cell proliferation was observed via CCK8 methods. Huh7 cells pre-treated with inhibitors were followed with HCV infection.The intracellular HCV RNA and protein levels were determined by quantitative PCR and immunofluorescence assay. Results:The absorbance values at 450 nm of 100 μmol/L QNZ treatment group（0.730±0.056）and 100 μmol/L CAPE treatment group（1.040 ±0.014）were lower than those of untreated group（1.190±0.040

P=0.000）. The proliferation level of each concentration of Lenalidomide treatment group（100 μmol/L treatment group

1.250±0.016）was similar with untreated group（P=0.306）. In terms of antiviral activity

the HCV RNA levels of 100 nmol/L Lenalidomide treatment group[（3.79 ±0.88）×105] and QNZ treatment group [（6.64 ±1.11）×105] were significantly lower than those of untreated group[（1.51±0.45）×106

P=0.000]. CAPE treatment group[（1.61±0.15）×106] had a similar HCV RNA level with untreated group（P=0.383）. Conclusion:TNF-α inhibitor Lenalidomide is less toxic to cells and can inhibit hepatitis C virus infection in hepatocytes.