PSD-95结构域PDZ1过表达拮抗缺氧缺糖诱导的海马神经元凋亡

为了观察突触后致密物质-95（postsynaptic density95，PSD-95）结构域PDZI过表达对缺氧缺糖诱导的海马神经元凋亡的影响，本研究采用培养21d的Sprague—Dawley大鼠海马神经元，加入PDZ2腺病毒颗粒感染24h，收集细胞进行免疫沉淀、免疫印迹实验；缺氧缺糖1．5h后，用DAPI染色后荧光显微镜观察细胞凋亡，并收集细胞进行免疫印迹实验。结果显示：（1）PDZ2在海马神经元中过表达；（2）过表达的PDZ1使缺氧缺糖诱导的海马神经元凋亡数量减少（P〈0．05）；（3）过表达的PDZ1使PSD-95与GluR6结合减少；（4）PDZ1过表达抑制由缺氧缺糖诱导的火鼠海马神经元MLK3和JNK1／2磷酸化。以上结果提示，PDZ1过表达能拈抗缺氧缺糖诱导的海马神经元凋亡。

Overexpression of PDZ1 domain of PSD-95 protein rescues hippocampl neurons from apoptosis induced by oxygen-glucose deprivation

To detect the effect of PDZ1,domain of postsynaptic density 95(PSD-95),on apoptosis of hippocampal neurons induced by oxygen-glucose deprivation(OGD),Sprague-Dawley rat hippocampal neurons were infected with PDZ1-viruses after 21 days of plating.Twenty-four hours after infection,cells were treated with OGD for 1.5 h,then were incubated with DAPI and apoptosis-like cells were characterized,or were collected for co-immunoprecipitation and Western blot analyses.The results showed that:(1) PDZ1 overexpression w...