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目的 探讨亚低温对大鼠脑缺血后神经元凋亡的影响 ,揭示亚低温的部分神经保护机制。方法 采用“双侧颈总动脉阻断 +全身低血压”方法来建立大鼠短暂性全脑缺血模型。用神经元尼氏体亚甲兰特殊染色法观察大鼠脑缺血后海马CA1区神经元损害情况 ;原位细胞凋亡检测法 (TUNEL染色 )及电镜观察脑缺血后CA1区神经元凋亡情况。结果 与假手术组、低温缺血组相比 ,常温缺血组海马CA1区神经元缺失明显 (P <0 .0 1)。常温及低温缺血组海马CA1区均存在神经元凋亡 ,但低温缺血组海马CA1区凋亡神经元数明显少于常温缺血组 (P <0 .0 1)。结论 经“双侧颈总动脉阻断 +全身低血压”方法建立的大鼠短暂全脑缺血模型证实了亚低温的脑保护作用。全脑缺血后的迟发性神经元死亡很可能经由凋亡途径 ,而亚低温可通过抑制缺血性神经元凋亡而发挥一定的神经保护作用
Objective To investigate the effects of mild hypothermia on the neuronal apoptosis after cerebral ischemia in rats and to reveal some neuroprotective mechanisms of mild hypothermia. Methods The method of “bilateral common carotid artery occlusion + systemic hypotension” was used to establish a transient global cerebral ischemia model in rats. Neuronal damage of hippocampal CA1 region was observed by Nissl sub-methylene blue staining of neurons. TUNEL staining and electron microscopy were used to observe the changes of neuron apoptosis in hippocampal CA1 area Death situation. Results Compared with sham operation group and hypothermia group, neurons in hippocampal CA1 area of normal temperature group were significantly decreased (P <0.01). The apoptosis of hippocampal CA1 region was observed in both normal and hypothermic groups, but the number of apoptotic neurons in hippocampal CA1 area of hypothermic ischemia group was significantly less than that of normal temperature group (P <0.01). Conclusion The transient global cerebral ischemia model established by the method of “bilateral common carotid artery occlusion + systemic hypotension” confirmed the hypothermic brain protective effect. Delayed neuronal death after global cerebral ischemia is likely to be via the apoptotic pathway, whereas mild hypothermia exerts a neuroprotective effect by inhibiting ischemic neuronal apoptosis