| 摘要: |
| 目的揭示人脑急性创伤性脑损伤后Omi/HtrA2介导的神经细胞凋亡线粒体途径的激活。方法选择100例脑外伤开颅手术中获得的脑挫裂伤脑组织作为外伤组，另外选择100例脑出血患者手术径路中获得的正常脑组织作为对照组，采用流式细胞仪检测神经细胞凋亡，采用Western-blot检测Omi/HtrA2、X染色体连锁凋亡抑制蛋白（XIAP）、pro-caspase3、pro-caspase9和剪切聚腺苷二磷酸-核糖多聚酶（PARP）表达，采用四肽荧光底物法检测caspase3和caspase9活性。结果外伤组脑组织凋亡神经细胞比例、Omi/HtrA2、pro-caspase3、pro-caspase9和剪切PARP表达及caspase3和caspase9活性较对照组显著升高（均P＜0.01），外伤组脑组织XIAP表达较对照组显著下降（P＜0.01）。外伤组脑组织Omi/HtrA2表达与凋亡神经细胞比率、pro-caspase3、pro-caspase9和剪切PARP表达及caspase3和caspase9活性呈显著正相关（均P＜0.01），与XIAP表达呈显著负相关（P＜0.01）；外伤组脑组织XIAP表达与凋亡神经细胞比率、pro-caspase3、pro-caspase9和剪切PARP表达及caspase3和caspase9活性呈显著负相关（均P＜0.01）。结论Omi/HtrA2介导的线粒体途径可能参与人急性创伤性脑损伤后神经细胞凋亡过程。 |
| 关键词: 人类 创伤性脑损伤 神经细胞凋亡 Omi/HtrA2 |
| DOI：10.12056/j.issn.1006-2785.2017.39.20.2017-377 |
| 分类号: |
| 基金项目:浙江省医药卫生科技计划平台项目（2014ZDA019） |
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| Mitochondrial Omi / HtrA2 signaling pathway involved in neuronal apoptosis after cerebral contusion and laceration |
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Jiande First People's Hospital
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| Abstract: |
| Objective To investigate the effect of Omi/HtrA2 mediated mitochondrial signaling pathway in neuronal apoptosis after acute traumatic brain injury. Methods Brain tissue samples were collected during craniotomy from 100 patients with cerebral contusion and laceration (trauma group), and normal brain tissue samples were collected from 100 patients with intracerebral hemorrhage(control group). Flow cytometry was applied to determine apoptotic neuronal cells, Western-blotting was performed to test expressions of Omi/HtrA2, X-linked inhibitor of apoptosis protein (XIAP), pro-caspase-3, pro-caspase-9 and cleaved poly ADP-ribose polymerase (PARP), and four peptide fluorescence substrate method was employed to detect activities of caspase 3 and caspase 9 proteins. Results Percentage of apoptotic nerve cells, expressions of Omi/HtrA2, pro-caspase 3,
pro-caspase 9 and cleaved PARP as well as activities of caspase 3 and caspase 9 proteins were significantly higher and the expression of XIAP was significantly lower in brain tissues of trauma group than those in control group (all P＜0.01). In trauma group, expression of Omi/HtrA2 was positively correlated with percentage of apoptotic nerve cells, expressions of pro-caspase 3,
pro-caspase 9 and cleaved PARP as well as activities of caspase 3 and caspase 9 proteins, and negatively correlation with the expression of XIAP. The expression of XIAP was negatively correlated with percentage of apoptotic nerve cells, expressions of Omi/HtrA2, pro-caspase 3, pro-caspase 9 and cleaved PARP as well as activities of caspase 3 and caspase 9 proteins. Conclusion Omi/HtrA2 mediated mitochondrial signaling pathway may be involved in neuronal apoptosis after acute traumatic brain injury. |
| Key words: Human Traumatic brain injury Neuronal apoptosis Omi/HtraA2 |
