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目的:探讨早期高压氧(脑缺血再灌注30min后)对脑缺血再灌注神经细胞凋亡及学习与记忆的影响。方法:将实验用大鼠随机分为假手术组、模型组及处理组。采用Zea Longa法制作脑缺血再灌注动物模型,观察大鼠早期高压氧处理后神经功能缺损评分、海马区凋亡阳性细胞计数、caspase-3和Bcl-2蛋白表达的改变情况;并采用Morris水迷宫检测大鼠的逃避潜伏期(EL)和穿过原平台次数的变化。结果:第2h,1d,2d,3d大鼠神经功能缺损评分模型组和处理组均较假手术组增加(P<0.01),第2,3d大鼠神经功能缺损评分处理组较模型组明显降低(P<0.05);模型组凋亡细胞计数和caspase-3蛋白表达量显著多于假手术组(P<0.01),而处理组较模型组明显减少(P<0.01);模型组Bcl-2蛋白量较假手术组明显增加(P<0.01),处理组则更高于模型组(P<0.01);模型组EL时间比假手术组明显延长,穿过原平台次数明显少于假手术组(P<0.01),而处理组EL时间则较模型组明显缩短,穿过原平台次数则明显多于模型组(P<0.05)。结论:早期高压氧能抑制脑缺血再灌注损伤海马神经细胞的凋亡,提高学习记忆功能。
Objective: To investigate the effect of early hyperbaric oxygen (30 min after cerebral ischemia-reperfusion) on neuronal apoptosis, learning and memory after cerebral ischemia reperfusion. Methods: The rats were randomly divided into sham operation group, model group and treatment group. The animal model of cerebral ischemia-reperfusion was established by Zea Longa method. The neurological deficit scores, the number of apoptotic cells in hippocampus and the expressions of caspase-3 and Bcl-2 protein were observed after hyperbaric oxygenation in rats. Water maze test rats escape latency (EL) and the number of changes through the original platform. Results: Compared with the sham-operation group, the neurological deficit score of model group and the treatment group on the 2nd, the 1th, the 2nd and the 3rd days were significantly increased (P <0.01), and the neurological deficit score on the 2nd and 3rd day was significantly lower than the model group (P <0.05). The apoptotic cell count and caspase-3 protein expression in the model group were significantly higher than those in the sham-operation group (P <0.01), while those in the untreated group were significantly decreased (P <0.01) (P <0.01), and the treatment group was higher than the model group (P <0.01). The EL time of the model group was significantly longer than that of the sham-operated group and the number of passing through the original platform was significantly less than that of the sham operation group (P <0.01), while the treatment group EL time was significantly shorter than the model group, the number of crossing the original platform was significantly more than the model group (P <0.05). Conclusion: Hyperbaric oxygen can inhibit apoptosis of hippocampus neurons after cerebral ischemia-reperfusion injury and improve learning and memory.