Objective To investigate the Protective effect of propofol on the retinal ganglion cells of the rat optic nerve crush model. Methods 67 SD rats. Randomly selected 20 rats, don't do any processing for the normal group. With more than 47 rats optic clamps for optic nerve contusion model, legal system building 5 failure, success of 42 rats were randomly divided into the optic nerve damage and propofol group, 21/group. Will not be any treatment after optic nerve injury group building, 4 hours after propofol group for propofol therapy. After 4 days of successful modeling, the apoptosis of retinal ganglion cells were detected by TUNEL staining. After 7 days of successful modeling, the expression of Caspase-3, BCL-2 in retina and optic nerve cells of rats were detected by RT-PCR and Western-blot.After 14 days of successful modeling, The amplitude and latent period of P1 wave of flash visual evoked potential were detected.The animals were sacrificed and the optic nerve was taken to observe the pathological morphology of retina and optic nerve in rats, and the retinal ganglion cells (RGC) were counted. Results After 4 days of successful modeling,the apoptosis of the propofol group was significantly lower than that of the optic nerve injury group (P<0.05).After 7 days of successful modeling,the expression of Caspase-3 in the propofol group was significantly lower than that in the propofol group (P<0.05), the expression of BCL-2 in the propofol group was significantly higher than that in the propofol group (P<0.05).After 14 days of successful modeling, FG Positive RGC numbers:normal group>propofol group> optic nerve injury group and between groups difference was statistically significant (P<0.05). The flash visual evoked potential of the rats in propofol group was significantly shorter than that in the optic nerve injury group (P<0.05) and the amplitude of the visual evoked Potential was significantly higher than that of the optic nerve injury group (P<0.05).Conclusions Propofol treatment can through an early reduction in rats after optic nerve crush RGCs apoptosis, decreased Caspase-3 expression, increased BCL-2 expression and improve number of optic nerve crush of RGCs survival.