【摘要】 目的探讨脑出血(ICH)患者血肿周围组织神经元凋亡与凋亡相关基因Bcl2、Bax蛋白表达的关系。方法采用缺口末端标记法、免疫组化法分别检测ICH患者血肿周围组织神经元凋亡率和Bcl2、Bax表达水平,分析神经元凋亡率与Bcl2、Bax表达及Bax/Bcl2值的关系;出血量与Bcl2、Bax表达及Bax/Bcl2值的关系,以及神经元凋亡率与出血量、病程、神经功能缺损程度评分(NDS)的关系。结果ICH患者血肿周围组织神经元凋亡率及Bcl2、Bax表达明显高于正常对照组(均P<0.01);血肿周围组织神经元凋亡率与Bcl2表达呈负相关(r=-0.682,P<0.01),与Bax、Bax/Bcl2值表达呈正相关(r=0.592、0.740,均P<0.01)。出血量与血肿周围组织Bcl2表达呈负相关(r=-0.677,P<0.01),与Bax表达及Bax/Bcl2值呈正相关(r=0.654、0.751,均P<0.01)。细胞凋亡率与出血量及NDS呈正相关(r=0.829、0.897,均P<0.01),与病程不相关。结论细胞凋亡机制参与了ICH后继发性神经元损伤;Bcl2、Bax蛋白及Bax/Bcl2值对凋亡具有调控作用。更多还原

【Abstract】 Objective To study the relationship between neural apoptosis and the expression of Bcl-2,Bax proteins in the perihematomal brain tissue of patients with intracerebral hemorrhage(ICH).Methods The rate of neural apoptosis of perihematomal brain tissue was examined by TUNEL method and the Bcl-2,Bax proteins expression were detected by immunohistochemisty method. Correlation analysis was done not only for the expression of Bcl-2,Bax proteins and apoptosis rate with hematoma volume but also for the apoptosis rate with hematoma volume, the scores of clinical nervous impairment and the course of disease.Results The apoptosis rate and the expression of Bcl-2,Bax proteins in the perihematomal brain tissue of ICH patients significantly increased in comparison with the control group (all P<0.01).The expression rate of Bcl-2 protein showed obviously negative correlation to the apoptosis rate ( r=0.682, P<0.01)and the expression rate of Bax protein and the Bax/Bcl-2 ration showed obviously positive correlation to the apoptosis rate in perihematomal brain tissue of ICH patients ( r=0.740, P<0.01). The expression rate of Bcl-2 protein showed obviously negative correlation to the hematoma volume ( r=0.677, P<0.01) and the expression rate of Bax protein and the Bax/Bcl-2 ration showed obviously positive correlation to the hematoma volume in perihematomal brain tissue of ICH patients ( r=0.654,0.751,all P<0.01). The apoptosis rate showed obviously positive correlation to hematoma volume and the scores of clinical nervous impairment( r=0.829,0.897,all P<0.01),but uncorrelation to the course of disease.Conclusions The mechanism of apoptosis may be involved in the delayed neuron injure secondary ICH in human. Bcl-2 protein,Bax protein and Bax/Bcl-2 ration can regulate the period of apoptosis in ICH.更多还原