【摘要】 目的探讨创伤性脑损伤诱导神经细胞凋亡的机制。方法分别采用流式细胞术和借助caspase-3荧光分析试剂盒检测大鼠头颅打击伤后不同时间(3、12、24h和2、3、7、14d)损伤脑组织的神经细胞凋亡率和cas-pase-3活性的变化。结果损伤脑组织神经细胞凋亡率和caspase-3活性均随着伤后时间的延长而迅速增高,两者均至3d达峰值,分别为(14.6±2.4)%和(0.545±0.024)nmolAFC,然后逐渐下降,伤后14d分别下降到(3.2±0.8)%和(0.128±0.012)nmolAFC,但仍高于正常水平(P<0.01)。加入特异性caspase-3抑制剂z-DEVD-fmk后神经细胞凋亡率和caspase-3活性均显著降低(P<0.01)。结论caspase-3参与了创伤性脑损伤诱导的神经细胞凋亡。更多还原

【Abstract】 Objective To explore the mechanism of traumatic brain injury for inducing neuronal apoptosis.Methods At different times(3,12,24 h and 2,3,7,14 d)after traumatic brain injury,the rate of neuronal apoptosis was evaluated with flow cytometry and the caspase-3 activity in injured brain tissue was detected by caspase-3 fluorescent assay kit.Results After traumatic brain injury,both the rate of neuronal apoptosis and the caspase-3 activity increased rapidly.Three days after injury they reached the peak(14.6±2.4)%and(0.545±0.024)nmol AFC,respectively,then gradually fell down.The rate of neuronal apoptosis was(3.2±0.8)%and the caspase-3 activity was(0.128±0.012)nmol AFC 14 days after injury.But compared with the normal group,they were still significantly higher(P< 0.01).The four peptides inhibitor z-DEVD-fmk decreased significantly the rate of neuronal apoptosis and the caspase-3 activity(P< 0.01).Conclusion Caspase-3 is involved in neuronal apoptosis after traumatic brain injury.更多还原