DMT1过表达加重Aβ寡聚体诱导的细胞凋亡

DMT1 overexpression exacerbates Aβoligomer-induced cell damage

目的本研究旨在揭示金属离子转运蛋白DMT1在Aβ1-42寡聚体引起神经细胞毒性中的作用。方法将稳定过表达DMT1基因的SH-SY5Y细胞(S-DMT1)和过表达绿色荧光蛋白空质粒的SH-SY5Y细胞(SGFP)暴露于Aβ1-42寡聚体,采用CCK8和Heochst33258检测细胞的死亡率和凋亡率,Western blot检测凋亡相关因子Caspase-3、Bax和BCL2的水平。结果与SGFP细胞相比,S-DMT1细胞在Aβ1-42寡聚体处理后,活细胞数量显著降低,细胞发生核皱缩的比率显著高于SGFP组。而且Aβ1-42寡聚体作用后S-DMT1细胞Caspase-3、Bax蛋白水平均高于SGFP组,而BCL2下降。结论DMT1过表达促进细胞凋亡,增加Aβ1-42寡聚体的毒性作用。

Objective To study the role of metal ion transporter DMT1 in neurotoxicity induced by Aβ1-42 oligomers.Methods We exposed SH-SY5 Y cells(S-DMT1)stably overexpressing the DMT1 gene and SH-SY5 Y cells(SGFP)overexpressing empty green fluorescent protein to Aβ1-42 oligomers.CCK 8 and Hoechst 33258 were used to detect the cell death rate and apoptotic rate.Western blot was used to detect the levels of apoptotic proteins Caspase-3,Bax and BCL2.Results Compared with SGFP cells,the number of viable cells in S-DMT1 cells after Aβ1-42 oligomer treatment was significantly decreased,the rate of nuclear shrinkage in S-DMT1 cells treated with Aβ1-42 oligomer was significantly higher than that in SGFP group.Moreover,the levels of Caspase-3 and Bax proteins in S-DMT1 cells were higher than those in SGFP group,while BCL2 decreased after Aβ1-42 oligomers.Conclusion DMT1 overexpression increases the toxic effects of Aβ1-42 oligomers via promoting apoptosis.