超氧化物歧化酶
氧化应激
丙二醛
活力测定
SH-SY5Y型
谷胱甘肽过氧化物酶
化学
转染
三磷酸腺苷
分子生物学
生物化学
细胞凋亡
细胞生物学
生物
细胞培养
神经母细胞瘤
基因
遗传学
作者
Yongjian Zhou,Nanqu Huang,Yuanyuan Li,Zhisheng Ba,Yanjun Zhou,Yong Luo
出处
期刊:PeerJ
[PeerJ]
日期:2021-08-10
卷期号:9: e11978-e11978
被引量:3
摘要
The aim of this study was to investigate the effect of icaritin (ICT) on TAR DNA-binding protein 43 (TDP-43)-induced neuroblastoma (SH-SY5Y) cell damage and to further explore its underlying mechanisms.To investigate the possible mechanism, TDP-43 was used to induce SH-SY5Y cell injury. Cell viability was evaluated by the CCK-8 assay. The mitochondrial membrane potential (MMP) was determined with JC-1. The expression levels of TDP-43 and cytochrome C (CytC) were measuring by Western blotting. Changes in adenosine 5'-triphosphate (ATP) content, total antioxidative capacity (T-AOC), glutathione peroxidase (GSH-Px) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected with specific kits.The results showed that ICT reduced the cell damage induced by TDP-43. ICT reduced the expression level of TDP-43; increased ATP content and the MMP; decreased CytC expression; increased T-AOC and GSH-Px, total SOD (T-SOD), copper/zinc SOD (CuZn-SOD), and manganese SOD (Mn-SOD) activity; and decreased MDA content.The results suggest that ICT has a protective effect on TDP-43-transfected SH-SY5Y cells that is related to reductions in TDP-43 expression and mitochondrial damage and alleviation of oxidative stress.
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