The effects of autophagy on neuronal damage can be positive or detrimental negative. Through establishing a model of fetal rat cortical neuron hydraulic shock injury, dipotassium bisperoxo (picolinoto) oxovanadate (V) [bpv(pic)] was used to inhibit PTEN at different time points post-injury and autophagy level after neuronal injury was assessed. Neurons were divided into several intervention groups according to the time point at which bpv(pic) was used to inhibit autophagy, normal neurons and injuried neurons were set as two control groups. Growth of neurons in each group was assessed through immunofluorescence staining. Expression of the autophagy-related proteins LC3-II and LC3-I was analyzed by western blot. Expression of PTEN, mTOR and Beclin-1 was detected by RT-PCR. The number of autophagosomes in the normal group, injury control group and 24 h, 36 h intervention groups were assessed by electron microscope.

We found that autophagy was enhanced after neuronal injury and that the levels of LC3-II was significantly reduced by bpv (pic) intervention. The growth of the injury control groups was worse than normal groups, while improved through bpv(pic) intervention at 24 h and 30 h after injured. Western blot analysis showed that the LC3-II and LC3-II/LC3-I ratios of cells increased post-injury, and autophagy induction was evident by electron microscopy. These effects were confirmed by RT-PCR analysis. Taken together, these data suggest that autophagy is activated after injury in neurons while can be inhibited by bpv(pic) administration and then promote the repair of injured neurons.

自噬对神经元损伤的影响可以是积极的，也可以是有害的。通过建立胎鼠皮层神经元液压休克损伤模型，在损伤后不同时间点使用双过氧化氢（picolinoto）氧钒酸二钾（V）[bpv（pic）]抑制PTEN，评估神经元损伤后的自噬水平。根据使用bpv(pic)抑制自噬的时间点将神经元分为若干干预组，将正常神经元和损伤神经元设为两个对照组。通过免疫荧光染色评估每组神经元的生长。通过蛋白质印迹分析自噬相关蛋白 LC3-II 和 LC3-I 的表达。RT-PCR检测PTEN、mTOR和Beclin-1的表达。正常组自噬体的数量，

我们发现神经元损伤后自噬增强，并且通过 bpv (pic) 干预显着降低了 LC3-II 的水平。损伤对照组的生长情况比正常组差，但在受伤后24小时和30小时通过bpv(pic)干预有所改善。Western印迹分析显示，损伤后细胞的LC3-II和LC3-II/LC3-I比值增加，电镜下可见自噬诱导。这些影响通过 RT-PCR 分析得到证实。综上所述，这些数据表明自噬在神经元损伤后被激活，而 bpv(pic) 给药可以抑制自噬，然后促进受损神经元的修复。