摘要
建立了Aβ_(1-40)诱导的SH-SY5Y神经母瘤细胞损伤模型,并探讨了儿茶素对该细胞模型的保护作用及可能机制。采用四唑盐(MTT)法检测细胞存活能力、乳酸脱氢酶(LDH)法检测细胞膜的通透性变化,对Aβ_(1-40)的SHSY5Y细胞毒性及儿茶素的保护作用进行研究;并通过活性氧(ROS)试剂盒及Caspase 3活性检测试剂盒分别对Aβ_(1-40)损伤SH-SY5Y细胞的ROS水平及Caspase 3活性变化进行检测。结果发现儿茶素能够提高由Aβ_(1-40)引起的SH-SY5Y细胞存活能力下降,降低LDH的释放量,其作用机制可能与儿茶素能够降低Aβ_(1-40)诱导的细胞氧化水平及Caspase 3活性的升高有关。
In the present work, a SH-SY5Y injuring model induced by Aβ1-40 was established, and the effect and possible mechanisms of Catechin on the model were investigated. Cell viability was assayed by MTT, and membrane permeability was detected by the LDH kit. In addition, the ROS kit and Caspase 3 activity assay kit were employed to measure the ROS level and Caspase 3 activity in SH-SY5Y cell, respectively. The results showed that, Aβ1-40 decreased the cell viability and promoted the membrane permeability of SH-SY5Y, but Catechin could inhibit the impact of Aβ1-40. The possible mechanism involved is that Catechin might decrease the Oxidation level and Caspase 3 activity in SH-SY5Y cell.
作者
刘彦霞
王佳月
戴雪伶
孙雅煊
LIU Yan-xia;WANG Jia-yue;DAI Xue-ling;SUN Ya-xuan(Beijing Laboratory of Bioactive Substances and Functional Foods,Beijing Union University,Beijing 100191,China)
出处
《生物学杂志》
CAS
CSCD
北大核心
2018年第4期7-10,共4页
Journal of Biology
基金
北京市教育委员会面上项目(KM201611417002)
