首页> 外文期刊>European Journal of Histochemistry >Neural stem cell conditioned medium alleviates Aβsub25-35/sub damage to SH-SY5Y cells through the PCMT1/MST1 pathway
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Neural stem cell conditioned medium alleviates Aβsub25-35/sub damage to SH-SY5Y cells through the PCMT1/MST1 pathway

机译:神经干细胞条件培养基通过PCMT1 / MST1途径缓解Aβ 25-35损伤对SH-SY5Y细胞的损伤

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Alzheimer’s disease (AD) is a progressive, neurodegenerative disease. Accumulating evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue (substantia nigra, blue plaque, paraventricular nucleus). In this study, we investigated the effect of neural stem cell conditioned medium alleviates Aβsub25-35/sub damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβsub25-35/sub significantly decreased the cell viability in time and dose dependent manner. However, Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had inhibitory effect on toxicity when fibrillation of Aβsub25-35/sub occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβsub25-35/sub + NSC-CDM group. sh-PCMT1 significantly reduced the PCMT1, the cell viability and inhibited the protective effect; induced apoptosis and increased the expression of p-MST1. Overexpression of PCMT1 group reversed the effect of Aβsub25-35/sub inhibited the cell viability and Aβsub25-35/sub induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβsub25-35/sub to cells by increasing PCMT1, reducing MST phosphorylation.
机译:阿尔茨海默病(AD)是一种进步,神经变性疾病。累积证据表明,蛋白质异己酸盐甲基转移酶1(PCMT1)在脑组织中高度表达(基础NIGRA,蓝色斑块,椎间露核)。在这项研究中,我们研究了神经干细胞条件培养基通过PCMT1 / MST1途径缓解Aβ 25-35对SH-SY5Y细胞的损伤。结果表明,Aβ<亚> 25-35 以时间和剂量依赖性方式显着降低细胞活力。然而,当Aβ 25-35 在其存在和NSC-CDM发生抑制剂结果时,神经干细胞 - 完全培养基(NSC-CPM)或NSC-CDM对毒性有抑制作用。在Aβ 25-35 + NSC-CDM组中发现了PCMT1表达水平的增加。 SH-PCMT1显着降低了PCMT1,细胞活力并抑制了保护效果;诱导细胞凋亡并增加p-MST1的表达。 PCMT1组的过度表达逆转Aβ 25-35 抑制细胞活力和Aβ 25-35 诱导细胞凋亡的影响。总之,NSC-CDM通过增加PCMT1来校正Aβ 25-35 对细胞的损伤,降低MST磷酸化。

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