动物造模 z-bio 2022-04-29 681

　　Objective: To investigate the effect and mechanism of propofol intervention on the injured optic nerve and retinal ganglia after optic nerve injury in rats.

　　Methods: There were 67 SD rats, 20 were randomly selected as the normal group, and were not given any treatment. The remaining optic nerve clamping method was used for modeling, and 42 rats were successfully included in the experiment. They were randomly divided into model control group and propofol group, with 21 animals in each group. 4 days after modeling, TUNEL method was used to detect the apoptosis of rat retina and optic nerve cells, and 7 days after modeling, RT-PCR and Western-blot were used to detect the gene and protein expressions of Caspase-3 and BCL-2 in retina and optic ganglion cells. . 14 days after model establishment, flash visual evoked potentials were detected, the rats were sacrificed, and the eyeballs were removed. The pathological morphology of retina and optic nerve was observed, and retinal ganglion cells were counted.

　　Results: 4 days after modeling, the number of apoptotic retinal ganglion cells in the propofol group was significantly lower than that in the model control group (P<0.05). The expression of BCL-2 was significantly decreased (P<0.05); the expression of BCL-2 was significantly increased (P<0.05). 14 days after modeling, the number of fluorescent gold-positive RGCs was the least in the model control group, more in the propofol group, and the most in the normal group, and there was a statistically significant difference between the groups (P<0.05). The flash visual evoked potential duration of the propofol group was shorter than that of the model control group (P<0.05), and the amplitude was significantly higher than that of the model control group (P<0.05).

　　Conclusion: Propofol intervention can protect the optic nerve injury by reducing the apoptosis of RGCs after optic nerve clamping, reducing the expression of retinal Caspase-3 and increasing the expression of BCL-2.