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目的:探讨低氧预处理对大鼠海马神经元缺氧性神经突触损伤的保护作用及其机制。方法:(1)将成年雄性Wistar大鼠或培养的新生大鼠海马神经元分别随机分为三组:对照组、缺氧组和低氧预处理组。麻醉后分别取海马切片,进行CA3区Schaffer侧支刺激,记录CA1区椎体细胞诱发电位的变化。(2)将新生大鼠海马神经元培养7-11d,分组处理后,用免疫组织化学染色方法检测三组海马神经元c-fos蛋白表达变化并进行光密度分析。结果:经低氧预处理后,可以使海马脑片的群峰电位在缺氧后开始减小、完全消失的时间出现延迟,分别为(4.52±0.99)min和(9.04±1.93)min,与缺氧组比较差异有统计学意义(P<0.05);培养的海马神经元c-fos表达阳性率显著性降低、平均光密度值显著性减少(P<0.05)。结论:低氧预处理可以延缓缺氧对大鼠海马神经突触的抑制作用,这种保护作用可能与神经元c-fos表达减少有关。
Objective: To investigate the protective effect and mechanism of hypoxic preconditioning on hypoxic neuronal synaptic damage in rat hippocampal neurons. Methods: (1) Adult male Wistar rats or cultured neonatal rat hippocampal neurons were randomly divided into three groups: control group, hypoxia group and hypoxic preconditioning group. Hippocampal slices were obtained after anesthesia, Schaffer collateral stimulation in CA3 area was performed, and the changes of evoked potentials in CA1 area were recorded. (2) The hippocampal neurons of neonatal rats were cultured for 7-11 days. After the treatment, the expression of c-fos protein in three groups of hippocampus neurons was detected by immunohistochemical staining and the optical density was analyzed. Results: After hypoxic preconditioning, the peak potentials of hippocampal slices began to decrease after hypoxia, and disappeared completely (4.52 ± 0.99) min and (9.04 ± 1.93) min, respectively The difference was statistically significant (P <0.05). The positive rate of c-fos expression in cultured hippocampal neurons decreased significantly and the average optical density decreased significantly (P <0.05). CONCLUSION: Hypoxic preconditioning can delay the inhibitory effect of hypoxia on neuronal synapse in hippocampus of rats, which may be related to the decrease of c-fos expression in neurons.