Objective:To investigate the possible mechanisms of apoptosis occurred in islet β-cell line (INS-1) which was induced by PCB1254 in vitro. Methods:After the treatment with different concentrations of PCB1254,the cell viability of INS-1 was assayed by CCK-8. After the treatment with PCB1254 (5 μg/ml),the morphological change and apoptosis situation of INS-1 were observed by inverted microscope. The apoptosis of INS-1 was further detected by flow cytometry. The expression of Caspase-3,Bim,Bcl-2,C-Fos,P-JNK,P-P38 and P-ERK were measured by Western blot. Reactive oxygen species (ROS) level was detected by dihydroethidium (DHE) fluorescence probe. The apoptosis level of INS-1 was observed under inverted microscope after ERK inhibitor PD98059 intervening the PCB1254 treated INS-1 cells. Results:With the increasing of concentration of PCB1254,the cell viability of INS-1 declined. When the concentration was higher than 5 μg/ml,there were significant differences compared with the control group (P < 0.01). INS-1 cells apoptosis, which was induced by PCB1254 (5 μg/ml), was observed through inverted microscope. The apoptosis cells turned dark and floated in the medium. Flow cytometry assay showed that PCB1254 could induce the apoptosis of INS-1 cells. Western blot showed that the expressions of apoptosis related Cleaved Caspase-3 and Bim proteins were up-regulated,while the expression of anti-apoptotic protein Bcl-2 was down-regulated. The expression of oxidative stress related protein C-Fos was up-regulated and the ROS fluorescence was enhanced. The expression of p-ERK in MAPK signal pathway was up-regulated. No obvious change of apoptosis was found under the intervention of ERK inhibitor PD98059. Conclusion:PCB1254 may induce the apoptosis of INS-1 cells through oxidative stress signaling pathway,and this process may be accompanied with the activation of ERK signaling pathway.