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脑创伤后bcl—2蛋白的神经保护作用
引用本文:骆纯,朱诚,卢亦成,江基尧,张光霁. 脑创伤后bcl—2蛋白的神经保护作用[J]. 中国临床神经外科杂志, 2003, 8(3): 196-198
作者姓名:骆纯  朱诚  卢亦成  江基尧  张光霁
作者单位:第二军医大学长征医院神经外科,上海,200003
基金项目:军队"九五"指令性课题(96L036)
摘    要:目的 探讨液压脑损伤后凋亡抑制基因bcl—2的变化规律及bcl—2基因在创伤性脑损伤后细胞凋亡中的作用。方法 应用免疫组化观察大鼠中型液压脑损伤伤前及伤后6h、12h、1d、3d、7dbcl—2蛋白表达情况,应用TUNEIL和电镜观察伤后细胞死亡的形态。结果 免疫反应阳性细胞主要位于伤侧大脑半球皮质、皮层下白质、海马CAl、CA3及齿状回的神经元和神经胶质细胞,以海马CA3区最为显。在高倍镜下,表达Bcl—2蛋白的神经细胞胞核形态正常,很少见到凋亡或坏死的形态特征。伤后早期(6h),打击侧海马CA3区Bcl—2蛋白表达显下降;Bcl—2早期改变出现在伤后6h,比细胞凋亡提前表现;伤后l—3h,Bcl—2的表达下降相对缓慢。结论 bcl—2蛋白在抑制脑创伤后细胞凋亡中起重要作用,bcl—2可能是一种可诱导的神经保护因子。

关 键 词:创伤性脑损伤 细胞凋亡 bcl—2 表达
文章编号:1009-153X(2003)03-0196-03
修稿时间:2001-07-26

Protective Effect of bcl-2 Protein on Neurons following Experimental Traumatic Brain Injury in Rats
LUO Chun,ZHU Cheng,LU Yi-cheng,et al.. Protective Effect of bcl-2 Protein on Neurons following Experimental Traumatic Brain Injury in Rats[J]. Chinese Journal of Clinical Neurosurgery, 2003, 8(3): 196-198
Authors:LUO Chun  ZHU Cheng  LU Yi-cheng  et al.
Affiliation:LUO Chun,ZHU Cheng,LU Yi-cheng,et al.Department of Neurosurgery,Changzheng Hospital,Second Military Medical University,PLA,Shanghai200003,China
Abstract:Objective To investigate the change in bcl-2,a gene inhibiting apoptosis and its role in neuronal apoptosis following traumatic brain injury(TBI).Method Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPI)of moderate severity.Bcl-2protein expression in brain tissue was detected by immunohistochemistry before the FPI and6,12,24,72,148hours after FPI.The neuronal apoptosis in the brain were detected by TUNEL and election microscope.Results Bcl-2expression was observed in the cerebral cortex,subcortical white matter,dentate gyrus,and hippocampal CA1and CA3ipsilateral to injured hemisphere.Bcl-2positive neurons displayed normal nuclei morphology;The morphological features of apoptosis or necrosis in few Bcl-2positive neurons were observed.The immunoreactivity of Bcl-2protein decreased significantly in the hippocampus ipsilateral to the impacted site as early as6h after the TBI as compared with that before the TBI.The decrease in bcl-2protein expression became relatively slow from1to3hours after TBI.Conclusion Bcl-2may play an important role in inhibiting apoptosis after TBI and may be an inducible factor protecting the neurons in the CNS.
Keywords:Traumatic brain injury  Apoptosis  Bcl-2protein  Expression
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