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目的观察丰富环境(EE)对缺氧缺血性脑损伤(HIBD)Akt信号通路及大鼠海马神经元的影响。方法健康7日龄SD大鼠90只,随机均分为3组:正常对照(A)组,不建立模型,不给刺激;缺氧缺血非刺激(B)组,采用Sale法建立HIBD模型,但不给丰富环境刺激;丰富环境刺激(C)组,建立HIBD模型,术后给予EE刺激,2h/次,1次/d,共20d。分别在缺氧缺血后第3天和第20天各组随机选10只,断头取脑,分别采用免疫印迹和焦油紫染色的方法检测大鼠脑缺氧缺血后海马CA1区Akt和Bad(ser136)的磷酸化及神经元凋亡情况。结果与A组比较,B组第3天脑组织中Akt和Bad(ser136)的磷酸化程度显著降低(P<0.05),第20天海马神经元损伤非常严重(P<0.05)。C组Akt和Bad(ser136)的磷酸化程度显著高于B组(P<0.05),海马神经元损伤明显减轻(P<0.05)。结论EE刺激可以促进HIBD恢复,减少海马CA1区神经元损伤;Akt和Bad(ser136)磷酸化程度升高可能是其机制之一。
Objective To observe the effects of enriched environment (EE) on Akt signaling pathway and hippocampal neurons in hypoxic-ischemic brain damage (HIBD) rats. Methods Ninety healthy 7-day-old SD rats were randomly divided into three groups: normal control group (A), no model and no stimulation; hypoxic-ischemic non-stimulation group (B) , But not to enrich the environment; rich environment stimulation (C) group, the establishment of HIBD model, after giving EE stimulation, 2h / time, 1 time / d, a total of 20d. Ten rats were randomly selected from each group on day 3 and day 20 after hypoxia and ischemia, respectively, and the brain was decapitated. The expression of Akt and cTn in hippocampal CA1 area were detected by Western blotting and tar violet staining respectively Phosphorylation and Neuronal Apoptosis of Bad (ser136). Results Compared with group A, the phosphorylation of Akt and Bad (ser136) in brain tissue of group B was significantly decreased on the 3rd day (P <0.05). On the 20th day, the damage of hippocampal neurons was very serious (P <0.05). The phosphorylation of Akt and Bad (ser136) in group C was significantly higher than that in group B (P <0.05), and the damage of hippocampal neurons was significantly reduced (P <0.05). Conclusion EE stimulation can promote the recovery of HIBD and reduce the damage of neurons in hippocampal CA1 region. Elevated phosphorylation of Akt and Bad (ser136) may be one of the mechanisms.