文章摘要
朱柳迪，左成超，谷中娅，黄雅琪，曹幻，王芙蓉.光刺激对抑郁模型小鼠的神经保护作用及机制研究[J].神经损伤功能重建,2022,17(2):63-67
光刺激对抑郁模型小鼠的神经保护作用及机制研究
Neuroprotective Effect and Mechanism of Photic Stimulation on Depression Model Mice
  
DOI：
中文关键词: 抑郁症  光刺激  突触可塑性  脑源性神经营养因子  糖原合酶激酶-3β
英文关键词: depression  photic stimulation  synaptic plasticity  brain-derived neurotrophic factor  glycogen synthase kinase-3β
基金项目:国家重点研发计划 （No.2020YFC2006 001）； 国家自然科学基金 面上项目（No. 819 74218）； 华中科技大学自主 创新基金（No. 500 3540083）； 国家科技基础资源 调查专项（No. 201 8FY100900）； 湖北省重点研发计 划（No. 2020BCA0 89）
作者单位
朱柳迪，左成超，谷中娅，黄雅琪，曹幻，王芙蓉 华中科技大学同济 医学院附属同济医 院神经内科 
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中文摘要:
      目的：探究光刺激对抑郁模型小鼠的神经保护作用，并探究其可能的分子机制。方法：建立改良强迫 游泳抑郁模型，给予光刺激（频率40 Hz、占空比50%、照度500 Lux）治疗28 d。用悬尾试验、强迫游泳试验 和旷场试验评估小鼠的抑郁和焦虑样行为。Western blot检测小鼠前额叶皮质和海马突触相关蛋白及相关 信号通路蛋白的表达情况。结果：行为学测试结果表明强迫游泳成功诱导了小鼠抑郁模型，光刺激显著改 善了抑郁模型小鼠的抑郁和焦虑样行为。Western blot检测结果显示抑郁模型小鼠前额叶皮质中，突触后 致密蛋白95（PSD95）和NMDA 受体（NR）1、NR2A和NR2B蛋白水平降低，海马中PSD95、NR2A和NR2B 蛋白水平降低；光刺激可提高上述蛋白的表达水平。抑郁模型小鼠前额叶皮质和海马脑源性神经营养因子 （BDNF）表达降低，蛋白激酶B（AKT）表达降低、磷酸化水平降低，糖原合酶激酶-3β（GSK-3β）磷酸化水平 降低，光刺激可逆转上述转变。结论：光刺激有助于改善抑郁模型小鼠的抑郁样行为、增强突触可塑性，且 其神经保护作用可能至少部分通过激活BDNF/AKT/GSK3β信号通路实现。
英文摘要:
      We explored the therapeutic effect of photic stimulation (PS) on depression model mice and investigated its possible molecular mechanism. Methods: Mice were subjected to 5 days of forced swimming (FS) to establish a model of depression. They then received PS (frequency 40 Hz, duty cycle 50%, illumination 500 Lux) for 28 days. Depression- and anxiety-like behaviors in mice were assessed using the tail suspension test, forced swim test, and open field test. Western blot was used to detect the expression of synapse-related proteins and related signaling pathway proteins in the prefrontal cortex and hippocampus. Results: Behavioral results indicated that FS successfully induced a depression-like state in mice and that PS improve depressionand anxiety-like behaviors. Western blot showed that, in depression model mice, the levels of postsynaptic density protein 95 (PSD95), NMDA receptor (NR) 1, NR2A, and NR2B in the prefrontal cortex were decreased; the levels of PSD95, NR2A, and NR2B in the hippocampus were decreased. PS was able to restore the expression of the above proteins. The depression model mice prefrontal cortex and hippocampus also displayed a decrease in the expression of brain-derived neurotrophic factor (BDNF) and protein kinase B (Akt) and decreased hosphorylation level; PS was able to reverse the above effects. Conclusion: PS alleviates depression-like behavior and increases synaptic plasticity in depression model mice. Its neuroprotective effect may be achieved at least in part via the BDNF/AKT/GSK3β pathway.
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