BDNF对缺糖缺氧小鼠伏隔核中突触前膜蛋白Synapsin-1的影响
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摘要
目的探讨BDNF在缺糖缺氧复灌条件下对小鼠伏隔核突触前膜蛋白Synapsin-1的影响。方法 2017年12月—2018年2月,徐州医科大学麻醉学重点实验室将18只小鼠随机平均分为正常组(伏隔核脑片低糖DMEM培养基培养)、缺糖缺氧复灌组(伏隔核脑片EBSS培养基培养15 min后复灌1 h)、缺糖缺氧复灌给药组(伏隔核脑片EBSS培养基中加入BDNF培养15 min钟后复灌1 h)。给与相应的处理后,对Synapsin-1蛋白表达量进行测定。结果正常组Synapsin-1蛋白的相对表达量为(1.191 02±0.068 371),缺糖缺氧复灌组Synapsin-1蛋白的相对表达量为(0.791 935±0.093 63),缺糖缺氧复灌给药组Synapsin-1蛋白的相对表达量为(1.065 35±0.075 595)。缺糖缺氧复灌组与正常组相比Synapsin-1蛋白的相对表达量降低,差异有统计学意义(P<0.01),缺糖缺氧复灌给药组与缺糖缺氧复灌组相比Synapsin-1的蛋白相对表达量升高,差异有统计学意义(P<0.05)。缺糖缺氧复灌给药组与正常组相比Synapsin-1的蛋白相对表达量差异无统计学意义(P>0.05)。结论缺糖缺氧对伏隔核中神经元突触有损伤作用,BDNF对其神经元突触起到保护作用。
Objective To explore the effect of BDNF on synapsin-1 in NAc slices under the condition of oxygen-glucose deprivation. Methods 18 mice were selected from December 2017 to February 2018 in Jiangsu Province Key Laboratory of Anesthesiology in Xuzhou Medical University, and randomly divided into normal group(culture of low-glucose DMEM medium in nac slices), OGD/R group(culture of EBSS medium 15 minutes after reperfusion 1 hours in NAc slices) and OGD/R+BDNF group(culture of EBSS medium adding BDNF 15 minutes after reperfusion 1 hour in NAc slice). After treatment, the expression of synapsin-1 protein was determined. Results The relative expression of synapsin-1 protein in normal group was(1.191 02±0.068 371), and the relative expression of synapsin-1 protein in hypoxia-reperfusion group was(0.791 935±0.093 63), the relative expression of synapsin-1 protein in the drug-deficient hypoxia-reperfusion group was(1.065 35±0.075 595).There was a statistically significant difference in the relative expression of synapsin-1 protein in the OGD/R group compared with the normal group(P <0.01), and there was a statistically significant increase in the protein relative expression of synapsin-1 in the OGD/R+BDNF group and OGD/R group(P<0.05). There was no statistically significant difference in synapsin-1 protein relative expression between OGD/R+BDNF group and normal group(P>0.05). Conclusion Oxygen-glucose deprivation has a damaging effect on synaptic synapses in NAc brain region, and BDNF plays a protective role in neuronal synapses.
Objective To explore the effect of BDNF on synapsin-1 in NAc slices under the condition of oxygen-glucose deprivation. Methods 18 mice were selected from December 2017 to February 2018 in Jiangsu Province Key Laboratory of Anesthesiology in Xuzhou Medical University, and randomly divided into normal group(culture of low-glucose DMEM medium in nac slices), OGD/R group(culture of EBSS medium 15 minutes after reperfusion 1 hours in NAc slices) and OGD/R+BDNF group(culture of EBSS medium adding BDNF 15 minutes after reperfusion 1 hour in NAc slice). After treatment, the expression of synapsin-1 protein was determined. Results The relative expression of synapsin-1 protein in normal group was(1.191 02±0.068 371), and the relative expression of synapsin-1 protein in hypoxia-reperfusion group was(0.791 935±0.093 63), the relative expression of synapsin-1 protein in the drug-deficient hypoxia-reperfusion group was(1.065 35±0.075 595).There was a statistically significant difference in the relative expression of synapsin-1 protein in the OGD/R group compared with the normal group(P <0.01), and there was a statistically significant increase in the protein relative expression of synapsin-1 in the OGD/R+BDNF group and OGD/R group(P<0.05). There was no statistically significant difference in synapsin-1 protein relative expression between OGD/R+BDNF group and normal group(P>0.05). Conclusion Oxygen-glucose deprivation has a damaging effect on synaptic synapses in NAc brain region, and BDNF plays a protective role in neuronal synapses.
引文
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[3]刘志娟.脑源性神经营养因子在突触可塑性中的作用[J].国际神经病学神经外科学杂志,2015,42(2):185-188.
[4]Koyama Y,Tsujikawa K,Matsuda T,et al.Intracerebr oventricular administration of an endothelin ETB receptor agonist increases expressions of GDNF and BDNF in rat brain[J].European Journal of Neuroscience,2015,18(4):887-894.
[5]Luo L,Liu X L,Li J,et al.Macranthol promotes hippocampal neuronal proliferation in mice via BDNF-Trk B-PI3K/Akt signaling pathway[J].European Journal of Pharmacology,2015(762):357-363.
[6]Sasi M,Vignoli B,Canossa M,et al.Neurobiology of local and intercellular BDNF signaling:[J].Pflügers ArchivEuropean Journal of Physiology,2017,469(5):1-18.
[7]刘荣国,林星武,方向宇,等.背根神经节脉冲射频对神经病理性痛大鼠脊髓IRF8和伏隔核BDNF表达的影响[J].中华麻醉学杂志,2017,37(5):540-543.
[8]杜成昊,万海同,周惠芬,等.谷红注射液对新生乳鼠海马神经元缺氧缺糖损伤的保护作用[J].中华中医药杂志,2017(1):289-293.
[9]董梅,程树彬,郭彦芳,等.器官型脑片培养OGD复氧复糖模型中丁苯酞对于bcl-2/bax、及bim蛋白的调节作用[J].中风与神经疾病,2017,34(1):16-20.
[10]李钊,程树彬,郭彦芳,等.器官型脑片糖氧剥夺模型的建立[J].脑与神经疾病杂志,2017,25(11):707-710.
[11]Li M,Dai F R,Du X P,et al.Infusion of BDNF into the nucleus accumbens of aged rats improves cognition and structural synaptic plasticity through PI3K-ILK-Akt signaling[J].Behavioural Brain Research,2012,231(1):146.
[12]Jiang C,Lin W J,Sadahiro M,et al.VGF function in depression and antidepressant efficacy[J].Mol Psychiatry,2017.