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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 investigate the neuronal apoptosis and neurological changes in the injured area of glutamate carboxypeptidase Ⅱ (GCPⅡ) knockout mice and wild type C57BL / 6J mice after traumatic brain injury. Methods Twenty male C57BL / 6J mice were randomly divided into 4 groups (n = 10 in C57BL / 6J sham operation group, 10 sham operation group in GCPⅡ knockout mice, C57BL / 6J mice brain injury group 10, GCP Ⅱ gene knockout mouse brain injury group 10), using PinPointlTMPCI3000 precision cranial impact instrument, set the parameters (combat depth of 1.5mm, the strike time of 80ms, hit Speed of 1.5m / s), accurate impact on mouse cerebral cortex. Neurological scores, immunofluorescence staining and neuronal apoptosis in the surrounding area at 24h after injury were counted. Results Compared with C57BL / 6J mice, the number of neuronal apoptosis in GCPII knockout mice was significantly lower than that in C57BL / 6J mice (P <0.05). Conclusion After GCPⅡ gene knockout in mice, the number of apoptotic neurons in the peri-injured area after traumatic brain injury is significantly lower than that in C57BL / 6J mice and the neurological function is significantly improved, which further proves the protective effect of GCPⅡ knockout on the brain tissue after traumatic brain injury .