神经复元方对原代大鼠海马神经元BDNF/TrKB信号通路影响的研究

目的:研究神经复元方含药血清对原代大鼠海马神经元BDNF/TrkB信号通路及突触可塑性的影响,探讨治疗PSD的部分分子机制。方法:采用原代大鼠海马神经元氧化应激损伤模型,引入BDNF/TrkB通路抑制剂(K252a),分为正常对照组、H₂O₂培养组、含药血清+H₂O₂培养组、含药血清+K252a+H₂O₂组、K252a+H₂O₂组,用定量RT-PCR、免疫印迹法检测BDNF/TrkB信号通路相关蛋白(基因)表达水平,观察海马神经元突触的超微结构。结果:H₂O₂加入含药血清组突触密度增大,突触后致密物厚度增厚。SYNA、GAP-43和SYN1 mRNA水平和蛋白表达水平在含药血清+H₂O₂培养组比H₂O₂组明显提高(P<0.01)。突触相关蛋白在含药血清+K252a+H₂O₂组显著低于对照组和含药血清+H₂O₂培养组(P<0.01)。结论:神经复元方能修复海马神经元氧化应激损伤模型的突触可塑性,可能是通过介导BDNF/TrKB信号通路调节SYNI、SYNA基因,促进相关蛋白表达。

Study on the mechanism of Shenjing Fuyuan decoction effect of BDNF/TrkB signal pathway hippocampal neurons in model rats

Objective:To investigate the functional mechanism of Shenjing Fuyuan decoction in regulating BDNF/TrkB signal pathway to promote the synaptic plasticity of hippocampal neurons in the treatment of post-stroke depression.Methods:BDNF/TrkB pathway inhibitor(K252a)was introduced into primary rat hippocampal neuron oxidative stress injury model,which was divided into three groups,normal control group,H₂O₂ culture group,serum containing medicine + H₂O₂culture group,serum containing medicine+K252a+H₂O₂ group,K252a+H₂O₂ group.The expression level of BDNF/TrkB pathway-related protein(gene)was detected by quantitative RT-PCR and immunoblotting.Results: Serum containing medicine +H₂O₂ group of the synaptic density was increased.The mRNA level and protein expression level of SYNA、GAP-43、SYNI were significantly increased in the serum containing medicine +H₂O₂ group(P<0.01),compared with the H₂O₂ group.Synapse associated protein in serum containing medicine+K252a+H₂O₂ group was significantly lower than that in the control group and the serum containing medicine +H₂O₂ group(P<0.01).Conclusions:Shenjing Fuyuan decoction can repair the synaptic plasticity of oxidative stress injury model of hippocampal neurons,and its mechanism may be to regulate the gene of synaptic protein and promote the expression of SYNI and SYNA in hippocampus through BDNF/TrkB signal pathway.