脑源性神经营养因子对缺氧胚脑皮质神经元发挥保护作用的细胞内信号传导机制  

Intracellular Signaling Pathway of Neuroprotective Function of BDNF on Hypoxic-cultured Embryonic Neurons in Vitro

作　　者：孙小妹[1] 毛萌[1] 周晖[1] 罗小丽[1] 李胜富[2] 

机构地区：[1]四川大学华西第二医院儿科 [2]四川大学华西医院移植工程与免疫实验室,四川成都610041

出　　处：《华西医学》2006年第3期454-457,共4页West China Medical Journal

基　　金：国家自然科学基金资助(30371489);教育部科学技术研究重点项目(03133)

摘　　要：目的:通过胚脑皮质神经元的体外培养,探讨遭受缺氧刺激时,脑源性神经营养因子(Brain derivedneurotrophic factor,BDNF)对神经元发挥保护作用时所启动的细胞内信号传导通路。方法:对胚鼠皮质神经元进行体外培养,提取不同缺氧时间点单纯缺氧的对照组及BDNF干预组的细胞蛋白,采用免疫印记(western blotting)方法检测两组神经元在细胞外信号调节激酶(extracellular signal-related kinase,ERK1/2)/磷酸化ERK1/2、蛋白激酶Akt/磷酸化Akt、P38丝裂原活化蛋白激酶(P38 Mitogen-activated protein kinase,P38MAPK)/磷酸化P38MAPK表达上的差别。结果:与单纯缺氧组比较,加入BDNF可引起磷酸化ERK1/2和磷酸化AKT表达的增强,而磷酸化的P38MAPK在两组均没有表达。结论:BDNF引起磷酸化ERK1/2及磷酸化AKT表达的上调可能为BDNF发挥对缺氧神经元保护作用的机理之一。Objective： to investigate the possible signaling pathway of BDNF in protecting neurons from hypoxia - induced neurotoxicity. Methods： Grouping embryonic cortical neurons cultured in hypoxic environment with BDNF or without BDNF. Total proteins were extracted from different neuron groups. Then western blotting technique was used to examine the expression of ERK and phospho - ERK, Akt and phospho- Akt, P38MAPK and phospho - P38MAPK. Result： BDNF induced the increase of phosphorylation of ERK1/2 and Akt, and there was no change in total ERK, Akt and P38MAPK. Furthermore, Phosphorylation of P38MAPK could not be detected. Concolusion： The activation of ERK and Akt signaling pathway mediated BDNF＇neuroprotective function against hypoxic- induced neurotoxicity.

关 键 词：脑源性神经营养因子 胚脑皮质神经元 缺氧 ERK1/2 AKT 

分 类 号：R363[医药卫生—病理学]