丙泊酚,视神经损伤 z-bo 2020-11-12 389

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

　　Method: There are 67 SD rats, 20 of which are randomly selected as the normal group without any treatment. Yu Xing made the optic nerve clamp method, and 42 models were successfully included in the experiment. Randomly divided into: model control group and propofol group, each with 21 animals/group. 4 days after modeling, TUNEL method was used to detect the apoptosis of rat retina and optic nerve cells. 7 days after modeling, the expression of Caspase-3 and BCL-2 genes and protein in retina and optic ganglion cell tissues were detected by RT-PCR and Western-blot . 14 days after the model was established, flash visual evoked potentials were detected. The rats were sacrificed to take their eyeballs, and the pathological morphology of the retina and optic nerve of each group was observed, and the retinal ganglion cells were counted.

　　Results: 4 days after modeling, the number of apoptosis of retinal ganglion cells in the propofol group was significantly lower than that of the model control group (P<0.05). 7 days after modeling, the propofol group Caspase-3 The expression of BCL-2 was significantly reduced (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: the model control group was the least, the propofol group was more, and the normal group was the most, and the difference between the groups was statistically significant (P<0.05). The flash visual evoked potential period of propofol group rats was shorter than that of model control group (P<0.05), and the amplitude was significantly higher than model control group (P<0.05).

　　Conclusion: Propofol intervention can protect the optic nerve from damage by reducing the apoptosis of RGCs after optic nerve clamp in rats, reducing the expression of Caspase-3 in the retina, and increasing the expression of BCL-2.