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为了观察突触后致密物质-95(postsynaptic density 95,PSD-95)结构域PDZ1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PDZ1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)PDZ1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大鼠海马神经元MLK3和JNK1/2磷酸化。以上结果提示,PDZ1过表达能拮抗缺氧缺糖诱导的海马神经元凋亡。
In order to observe the effect of PDZ1 overexpression on PSD-95-induced apoptosis of hippocampal neurons in the postmortem density 95 (PSD-95) domain, a rat hippocampus of Sprague-Dawley rats The neurons were infected with PDZ1 adenovirus for 24h. The cells were harvested for immunoprecipitation and Western blotting. After hypoxia-deprivation and glucose deprivation for 1.5h, the cells were stained with DAPI and observed by fluorescence microscope. The cells were harvested and subjected to Western blotting. The results showed that: (1) PDZ1 was overexpressed in hippocampal neurons; (2) Overexpression of PDZ1 reduced the number of apoptotic hippocampal neurons induced by oxygen-glucose deprivation (P <0.05); (3) PSD-95 and GluR6 decreased; (4) Overexpression of PDZ1 inhibited the phosphorylation of MLK3 and JNK1 / 2 in hippocampal neurons induced by oxygen-glucose deprivation. The above results suggest that PDZ1 overexpression can antagonize hypoxia-glucose deprivation-induced apoptosis of hippocampal neurons.