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 Aβ25-35 damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβ25-35 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 Aβ25-35 occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβ25-35 + 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 Aβ25-35 inhibited the cell viability and Aβ25-35 induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβ25-35 to cells by increasing PCMT1, reducing MST phosphorylation.

中文翻译：

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神经干细胞条件培养基通过 PCMT1/MST1 通路减轻 Aβ25-35 对 SH-SY5Y 细胞的损伤。

阿尔茨海默病 (AD) 是一种进行性神经退行性疾病。越来越多的证据表明，蛋白质异天冬氨酸甲基转移酶 1 (PCMT1) 在脑组织（黑质、蓝斑、室旁核）中高度表达。在本研究中，我们研究了神经干细胞条件培养基通过 PCMT1/MST1 通路减轻 Aβ25-35 对 SH-SY5Y 细胞损伤的作用。结果表明，Aβ25-35 以时间和剂量依赖性方式显着降低细胞活力。然而，神经干细胞完全培养基（NSC-CPM）或NSC-CDM在存在Aβ25-35纤维化时对毒性具有抑制作用，NSC-CDM具有更好的抑制效果。在 Aβ25-35 + NSC-CDM 组中发现 PCMT1 表达水平增加。sh-PCMT1 显着降低了 PCMT1，细胞活力和抑制保护作用；诱导细胞凋亡并增加 p-MST1 的表达。PCMT1 组的过表达逆转了 Aβ25-35 抑制细胞活力和 Aβ25-35 诱导细胞凋亡的作用。总之，NSC-CDM通过增加PCMT1、减少MST磷酸化来纠正Aβ25-35对细胞的损伤。