摘要
目的:探讨CLU调控Tau进而参与阿尔茨海默病的可能发病机制。方法:1) 通过慢病毒转染人源性SH-SY5Y神经细胞构建CLU表达水平细胞模型,利用RT-qPCR、Western-blotting等方法检验细胞模型中CLU及Tau蛋白表达量。2) 利用QPCR技术在转录水平验证CLU的干扰和过表达,以及CLU干扰和过表达后对Tau的影响。结果:1) 利用CLU质粒转染至SH-SY5Y细胞中及正常SH-SY5Y细胞的cDNA为模板,通过RT-qPCR检测Tau在CLU过表达模型细胞中表达量明显高于正常组。2) 发现CLU的过表达同时会引起Tau表达量的增高,而CLU的干扰同时会引起Tau表达量的降低。结论:通过CLU质粒转染及过表达,调控Tau蛋白播散参与,从而引起阿尔茨海默病的发生。
Objective: To explore the possible mechanism by which CLU regulates Tau and participates in the pathogenesis of Alzheimer’s disease. Method: 1) A CLU expression level cell model was constructed by transfecting human SH-SY5Y neural cells with lentivirus, and the expression levels of CLU and Tau proteins in the cell model were tested using RT qPCR, Western blotting, and other methods. 2) Using QPCR technology to verify the interference and overexpression of CLU at the transcriptional level, as well as the impact of CLU interference and overexpression on Tau. Result: 1) Using CLU plasmid transfection into SH-SY5Y cells and cDNA from normal SH-SY5Y cells as templates, the expression level of Tau in CLU overexpression model cells was significantly higher than that in the normal group detected by RT qPCR. 2) It was found that overexpression of CLU can also cause an increase in Tau expression, while interference from CLU can also lead to a decrease in Tau expression. Conclusion: By transfecting and overexpressing the CLU plasmid, the diffusion of Tau protein is regulated, leading to the occurrence of Alzheimer’s disease.
出处
《临床医学进展》
2024年第5期567-575,共9页
Advances in Clinical Medicine
