Abstract: OBJECTIVE To investigate the protective effect of sulforaphane(SFN) on Adriamycin(ADM)-induced hepatocyte injury and its relationship with oxidative stress. METHODS Human normal liver cell(L02) and human hepatoma cell line(HepG2) were incubated in 96-well plates with different concentrations of SFN(6.25, 12.5, 25, 50, 100 μg·mL^-1) cultured for 48 h. Another HepG2 cells were added SFN(3.75, 7.5, 15, 31.25, 62.5, 125, 250, 500 μg·mL^-1), cultured for 24, 48 h. MTT assay was used to detect the cell inhibition rate. Calculated the 50% inhibitory concentration(IC₅₀ value). In vitro culture of L02, different concentration of SFN(3.75, 7.5, 15 μg·mL^-1) were added to the experimental group. 1.25 mg·mL^-1 ADM was added to the experimental group and the model group at 0.5, 1, 2, 3 h, respectively. Used the method of enzyme-linked immune in the cell culture supernatant of tumor necrosis factor-α(TNF-α), superoxide dismutase(SOD), malondialdehyde(MDA), lactate dehydrogenase(LDH) glucose transporter 4(GLUT4), nuclear factor NF protein-E2 related factor(Nrf2) determination of assessment. RESULTS SFN could significantly inhibit the in vitro proliferation of HepG2 in a drug concentration-effect and time-effect relationship. The inhibitory effect of SFN on L02 was relatively weak, and its IC₅₀ was 47.7 μg·mL^-1, which was significantly higher than that of HepG2. Compared with the model group, SFN could significantly decrease the level of MDA, LDH, GLUT4, TNF-α and the rate of apoptosis, increase the level of SOD, Nrf2 in the supernatant of cell culture. CONCLUSION SFN can significantly inhibit the proliferation of hepatocellular carcinoma cells in vitro, and has a selective inhibitory effect on it. Besides, SFN has a protective effect on ADM-induced hepatocyte injury. Through the Keap1-Nrf2/ARE pathway, biphasic antioxidant enzymes may be induced to eliminate carcinogens or other toxins in the body, therely reducing oxidative stress and inflammatory reaction in the liver tissue.