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作 者:韦祎 周沾 覃银莹 谢玉波[1] 利莉[1] Wei Yi;Zhou Zhan;Qin Yinying;Xie Yubo;Li Li(Anesthesiology Department,The First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China)
机构地区:[1]广西医科大学第一附属医院麻醉科,南宁530021
出 处:《广西医科大学学报》2022年第4期649-652,共4页Journal of Guangxi Medical University
基 金:国家自然科学基金资助项目(No.81373498);广西医科大学青年科学基金项目(No.GXMUYSF201811);广西自然科学基金重点项目(No.2020GXNSFDA238025);广西重点研发计划(No.桂科AB20159019);国家重点研发计划(No.2018YFC201905)。
摘 要:目的:评价异丙酚对胎鼠离体海马神经元脑源性神经营养因子(BDNF)表达的影响。方法:将SD大鼠腹中14 d胎鼠处死,分离海马组织,剪碎研磨,消化,吹打及离心。神经元体外培养至第8天,按随机数字表法分为3组:空白对照组(C组);20%脂肪乳剂对照组(I组)和100μmol/L异丙酚组(P组)。C组不做任何处理,I组加入20%脂肪乳剂,P组加入异丙酚孵育3 h至其终浓度为100μmol/L。采用免疫细胞化学法鉴定神经元并计算其纯度,CCK-8法检测神经元活性并绘制生长曲线,RTqPCR检测BDNF的mRNA表达量,Western blotting法检测BDNF蛋白的表达量。结果:与C组比较,P组神经元活性明显降低,BDNF的mRNA及蛋白表达量降低(P<0.05);I组神经元活力未见明显差异。结论:异丙酚通过下调BDNF对胎鼠海马神经元产生神经毒性作用。Objective:To assess the effect of propofol on the expression of brain-derived neurotrophic factor(BDNF)in hippocampal neurons of fetal rats in vitro.Methods:The 14-day-old fetal rats in the abdomen of SD rats were euthanize,and the hippocampal tissue was separated,chopped and ground,digested,blown and centrifuged.After cultured in vitro for 8 days,the neurons were randomly divided into blank control group(group C),20%lipid emulsion control group(group I)and 100μmol/L propofol group(group P).No treatment was given in group C,20%lipid emulsion was added in group I,and propofol was added in group P for 3 hours until the final concentration was 100μmol/L.The neurons were identified by immunocytochemistry and the purity was calculated.The neuron viability was detected by CCK-8 and the growth curve was drawn.The mRNA expression of BDNF was detected by qRT-PCR,and the expression of BDNF protein was detected by Western blotting.Results:Compared with group C,the activity of neurons and the expression of mRNA and protein of BDNF in group P were lower(P<0.05),but there was no significant difference in neuronal activity between group C and group I.Conclusion:Propofol has a neurotoxic effect on fetal rat hippocampal neurons by down-regulating BDNF.
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