中文摘要：

目的观察和探讨在铝致神经细胞死亡中,坏死抑制剂1（Nec-1）对凋亡和自噬的作用。方法用体外原代培养小鼠神经细胞的方法,制造铝损伤神经细胞模型,然后用细胞活力检测、荧光定量PCR（qRT-PCR）、蛋白印迹（Western-Blot）以及流式细胞术等方法从多角度对Nec-1的作用进行研究。结果①流式结果显示,在Al3＋（2mmol/L）作用于神经细胞后,随着Nec-1剂量的增加,细胞的凋亡率呈下降趋势,且差异有统计学意义（P〈0.05）;②qRT-PCR结果显示,以Al3＋（2mmol/L）为对照,Nec-1（60和90μmol/L）可使神经细胞的凋亡和自噬相关基因的表达呈显著性下降（P〈0.05）;③Western-Blot结果显示,同Al3＋（2mmol/L）组比,Nec-1（60和90μmol/L）组凋亡相关蛋白caspase-3的表达下降（P〈0.01）,Nec-1（30和60μmol/L）可使自噬相关蛋白LC3-Ⅱ表达下降（P〈0.05）。结论在本试验条件下,Nec-1可减少铝导致的神经细胞凋亡和自噬,起到保护神经细胞的作用。

英文摘要：

Objective To observe and investigate whether Nec-1 can inhibit apoptosis and autophagy death which occur on Al-induced nerve cells. Methods The present study was designed to manufacture Al injury model of nerve cells in vitro. Cell viability,qRT-PCR,western-blot and flow cytometry were used to reasearch and argument the role of Nec-1. Results The results presented here,indicated that ①after Al3 ＋ poisoning nerve cells and with Nec-1 dose increasing,the apoptosis rate of them declined（P 0. 05）; ② in comparison with Al3 ＋ （2 mmol /L） group,Nec-1 （60,90 μmol /L） enabled apoptosis and phagocytosis-related genes expression of nerve cells to reduce significantly（P 0. 05）;③compared with Al3 ＋ （2 mmol /L） group, Nec-1 （60,90 μmol /L） decreased the expression of apoptosis-related protein caspase-3 and autophagy-related protein expression of LC3-Ⅱ（P 0. 01）. Conclusions Nec-1 can reduce aluminum-induced apoptosis and phagocytosis of nerve cells and protect nerve cells accordingly.