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目的:研究热休克蛋白70(HSP 70)对大鼠心肺复苏后神经细胞凋亡的影响,探索HSP对脑复苏的可行性。方法:将46只成年Wistar大鼠随机分为假手术组、模型组与干预组,假手术组不进行模型制作及治疗干预;模型组仅制作心搏骤停(SCA)并心肺复苏动物模型,不进行治疗干预;干预组大鼠在SCA并心肺复苏模型制作后静脉注射HSP 70。分别于6、12 h后检测各组大鼠脑海马区神经细胞凋亡数目、Bcl-2蛋白表达量,对比分析各组大鼠神经细胞凋亡情况的差异,验证HSP 70对大鼠心肺复苏后神经细胞凋亡的保护作用。结果:HSP 70对大鼠心肺复苏后神经细胞具有保护作用,能减少神经元细胞凋亡数目,增加Bcl-2蛋白表达。结论:HSP 70对大鼠心肺复苏后神经细胞有保护作用,对脑复苏具一定的治疗前景。
Objective: To investigate the effect of heat shock protein 70 (HSP 70) on the apoptosis of neurons after cardiopulmonary resuscitation (CPR) in rats, and explore the feasibility of HSP for cerebral resuscitation. Methods: Forty-six adult Wistar rats were randomly divided into sham operation group, model group and intervention group. The model group and the sham operation group were not involved in the model preparation and treatment intervention. The model group was only used to establish cardiac arrest and cardiopulmonary resuscitation animal models, No treatment intervention was given; rats in the intervention group were given HSP70 intravenously after SCA and CPR models were made. The number of apoptotic neurons and the expression of Bcl-2 protein in hippocampus of rats in each group were detected at 6 and 12 h respectively. The apoptosis of neurons in each group was compared and the apoptosis of HSP70 was evaluated. Neuroprotective effects of apoptosis in post-neuronal cells. Results: HSP 70 had a protective effect on neurons after cardiopulmonary resuscitation in rats, which could reduce the number of neuronal apoptosis and increase the expression of Bcl-2 protein. Conclusion: HSP 70 has a protective effect on nerve cells after cardiopulmonary resuscitation in rats and has certain therapeutic prospects for cerebral resuscitation.