四乙胺对Aβ_(l-40)致伤的神经干细胞的存活及其Caspase-3表达的影响

The effects of tetraethyl-lammonium to the survival and Caspase-3 expression of Aβ_(l-40)-induced neural stem cells

目的探讨钾通道阻滞剂四乙胺(tetraethy-lammonium,TEA)在Aβl-40致伤的神经干细胞增殖及凋亡中的作用。方法 Aβl-40与神经干细胞共孵育,诱导神经干细胞损伤,以TEA作用于Aβl-40致伤的神经干细胞,利用MTT法和比色法分别检测神经干细胞在不同的时间点的存活率及Caspase-3活性。结果 Aβl-40可使神经干细胞的存活率降低,呈时间依赖性;Aβl-40与神经干细胞在不同的时间点共孵育后,Caspase-3活性逐渐增加,在24h达到高峰;加入TEA后,Aβl-40致伤的神经干细胞的存活率增加,Caspase-3活性表达下降。结论 Aβl-40对神经干细胞的致伤作用可能与钾通道的激活相关,TEA能够降低Aβl-40对神经干细胞的致伤作用,减少神经干细胞的凋亡为治疗阿尔茨海默病提供了新的方法。

[ Abstract ] Objective Using tetraethyl-lammonium （TEA）, this acts as a potassium channel blocker, to interfere the Aβ1-40-injured neural stem ceils （Aβ1-40-NSCS）. and observing the survival and Caspase-3 expres- sion of Aβ1-40-NSCS, we wants to know the effects of potassium channels blocker TEA in the proliferation and apoptosis of Aβ1-40-NSCS. Methods We incubated neural stem cells with Aβ1-40 （TEA）, which were known as the Aβ1-40-injured neural stem cells （Aβ1-40-NSCS）. Then the Aβ1-40NSCS were dealt with TEA. We measured the survival and Caspase-3 activity of A^3140-NSCS at different time points by MTr and colorimetric meth- ods. Results A certain concentration of A~,~ can reduce the survival of NSCS, which was time dependent. The Caspase-3 activity of the Aβ1-40-NSCS gradually increased and reached the peak at 24 h Caspase-3 activity. Treated with TEA, the survival rates of the Aβ1-40-NSCS increased and the expression of Caspase-3 activity de- creased. Conclusion Aβ1-40 can induce the injury of NSCS, resulting in decreased proliferation, survival and increased apoptosis of NSCS. The TEA, which acts as a potassium channel blocker, can reduce the injury effects of Aβ1-40 to NSCS and apoptosis of NSCS. Therefore, the injury effects of Aβ1-40 to NSCS may be related with the activation of pstassium ion channels, and the TEA may be a new molecule target of Alzheimer＇s disease.