Objective: To study the mechanism of toxic effect of polychlorinated biphenyls PCB1254 on retinal ganglion cells （RGC-5）. Methods: After RGC-5 cells were exposed to 0.125， 0.250， 0.500， 1.000 mg/L PCB1254， 0.01% methanol， and pure water， the level of miR-182 was detected in every group. In addition， by using the miR-182 mimics or miR-182 inhibitor to up-regulate or down-regulate the expression of miR-182 in RGC-5， apoptosis， proliferation，and cell cycle were observed. After the treatment with 0.5 mg/L and 1.0 mg/L PCB1254， miR-182 mimics were transfected into RGC-5 cells to observe the apoptosis and proliferation. Results: ① With the increasing concentration of PCB1254， the expression of miR-182 was declined. When the concentration was ≥0.5 mg/L， there were significant differences between experimental groups and the control group （P<0.05）. ② MiR-182 silencing led to increased Caspase-3 activity in RGC-5 cells， which indicated that miR-182 silencing promoted apoptosis （P<0.05）. CCK-8 assay showed that the cell viability was lower in miR-182 inhibitor group than that in the negative control group， which indicated that miR-182 silencing inhibited cell proliferation（P<0.05）. There were no significant differences in cell cycle between the negative control group and the miR-182 inhibitor group（P>0.05）. ③ When miR-182 were tranfected in RGC-5 exposed to 0.5 and 1.0 mg/L PCB1254， the caspase-3 activity decreased（P<0.05）, and cell viability increased （P<0.05）. It showed that miR-182 could improve the toxic effect of PCB1254 in cell apoptosis and proliferation. Conclusion: Our findings suggest that the PCB1254 may affect the proliferation and apoptosis of RGC-5 by inhibiting the expression of miR-182， which may lead to the damage of visual function.