论文部分内容阅读
目的:探讨知母皂苷(SAa B)对Aβ_(1-42)诱导的皮层神经元损伤是否有保护作用。方法:MTT法测皮层神经元细胞存活率;免疫荧光染色法检测神经元突触素(SYP)、突触后致密蛋白95(PSD-95)表达的改变。Western印迹法检测神经元SYP、PSD-95、p-Akt473、p-m TOR蛋白表达水平表达的改变。结果:Aβ_(1-42)作用48 h可使大鼠大脑皮层神经元细胞存活率明显降低,使神经元SYP、PSD-95、p-Akt473和p-m TOR蛋白表达明显降低。SAa B(0.01,0.1,1,5,10μmol/L)可明显对抗Aβ_(1-42)引起的神经元细胞存活率下降,并呈一定浓度依赖性。SAa B也可使SYP、PSD-95、p-Akt473和p-m TOR蛋白表达明显增加。结论:知母皂苷能够抑制Aβ_(1-42)诱导的皮层神经元突触损伤,这种作用可能与PI3K/Akt/m TOR信号转导通路有关。
Objective: To investigate whether SAa B can protect Aβ 1-42-induced cortical neuron injury. Methods: The survival rate of cortical neurons was determined by MTT assay. The expression of synaptophysin (SYP) and PSD-95 was detected by immunofluorescence staining. The expression of SYP, PSD-95, p-Akt473 and p-m TOR in neurons were detected by Western blotting. Results: Aβ_ (1-42) could significantly decrease the survival rate of neurons in cerebral cortex 48 h and decrease the expression of SYP, PSD-95, p-Akt473 and p-m TOR in neurons. SAa B (0.01,0.1,1,5,10μmol / L) significantly inhibited the neuronal cell viability induced by Aβ 1-42 and showed a concentration-dependent manner. SAa B also significantly increased the expression of SYP, PSD-95, p-Akt473 and p-m TOR protein. Conclusion: Tim saponin can inhibit the synaptic damage induced by Aβ 1-42, which may be related to the PI3K / Akt / m TOR signaling pathway.