小鼠GCPⅡ基因剔除对脑外伤后神经元的影响

Influence of mice GCPⅡ gene knockout on neuron after traumatic brain injury

目的研究谷氨酸羧肽酶Ⅱ(GCPⅡ)基因剔除小鼠和野生型C57BL/6J小鼠脑外伤后损伤周围区神经元的凋亡以及神经功能变化。方法雄性C57BL/6J小鼠随机20只,雄性GCPⅡ基因剔除小鼠随机20只,随机分为4组(C57BL/6J小鼠假手术组10只,GCPⅡ基因剔除小鼠假手术组10只,C57BL/6J小鼠颅脑损伤组10只,GCPⅡ基因剔除小鼠颅脑损伤组10只),应用PinPointlTM PCI3000精细颅脑撞击仪,设定参数(打击深度为1.5mm,打击时间为80ms,打击的速度为1.5m/s),精确撞击小鼠脑皮质。伤后24h行神经功能评分,免疫荧光染色,损伤周围区凋亡神经元计数。结果GCPII基因剔除小鼠较C57BL/6J小鼠外伤后神经功能明显改善(P<0.05);损伤周围区神经元凋亡数值较C57BL/6J小鼠组明显降低(P<0.05)。结论小鼠GCPⅡ基因剔除后,脑外伤后损伤周围区神经元凋亡数较C57BL/6J小鼠明显减少,神经功能明显改善,进一步证明小鼠GCPⅡ基因敲除后对脑外伤后脑组织的保护作用。

Objective To study changes of apoptosis neuron around the neuron injury area and nerve function between WT C57BL/6J mice and GCP Ⅱ gene knockout mice after traumanc brain injury. Methods A total of 9,0 male GCPⅡ gene knockout mice and 20 male wild- type C57BL/6J mice were used in this experiment. Gene knockout mice were randomly divided into two groups （KO ＋ TBI group, n= 10 ; KO ＋sham TBI group, n= 10）, and wild- type C57BL/6J mice were randomly divided into two groups （WT ＋ TBI group, n= 10 ; WT ＋ sham TBI group, n= 10）. TBI model was made by CCL Set the parameter（impact velocity 1. 5m/s, reaching depth 1.0mm,remained in the brain for 80ms）. 24h after TBI making neural function score, immunofluorescence staining ,neuron apoptosis counting around the brain injury area. Results Our results showed that GCP Ⅱ gene knockout mice administration improved neural function score and protected neuron around the brain injury area after 24h following TBI （P〈0. 05）. Conclusion Our findings suggest that GCP gene knockout exert its protective effect on brain by reducing neuron apoptosis.