Zheng Xiaolin, Hu Xiaoyan, Ge Tangdong, Li Mengdi, Shi Minxia, Luo Jincheng, Lai Hehuan, Nie Tingting, Li Fenglan, Li Hui
Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
J Biochem Mol Toxicol. 2017 Aug;31(8). doi: 10.1002/jbt.21920. Epub 2017 May 25.
Oxidative stress induces apoptosis in cardiac cells, and antioxidants attenuate the injury. MicroRNAs (miRNAs) are also involved in cell death; therefore, this study aimed to investigate the role of miRNAs in the effect of selenium on oxidative stress-induced apoptosis. The effects of sodium selenite were analyzed via cell viability, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) concentration. Flow cytometry was used to evaluate cell apoptosis. Fura-2AM was used to calculate intracellular Ca concentration. Sodium selenite could ameliorate hydrogen peroxide (H O )-induced cell apoptosis and improve expression levels of glutathione peroxidase and thioredoxin reductase. Pretreatment with sodium selenite improved SOD activity and reduced MDA concentration. Treatments with H O or sodium selenite decreased miR-328 levels. MiR-328 overexpression enhanced cell apoptosis, reduced ATP2A2 levels, and increased intracellular Ca concentration, while inhibition produced opposite effects. MiR-328 might be involved in the effect of sodium selenite on H O -induced cell death in H9c2 cells.
氧化应激诱导心肌细胞凋亡,而抗氧化剂可减轻这种损伤。微小RNA(miRNA)也参与细胞死亡;因此,本研究旨在探讨miRNA在硒对氧化应激诱导的细胞凋亡作用中的角色。通过细胞活力、超氧化物歧化酶(SOD)活性和丙二醛(MDA)浓度分析亚硒酸钠的作用。采用流式细胞术评估细胞凋亡。使用Fura-2AM计算细胞内钙浓度。亚硒酸钠可改善过氧化氢(H₂O₂)诱导的细胞凋亡,并提高谷胱甘肽过氧化物酶和硫氧还蛋白还原酶的表达水平。亚硒酸钠预处理可提高SOD活性并降低MDA浓度。用H₂O₂或亚硒酸钠处理会降低miR-328水平。miR-328过表达增强细胞凋亡,降低ATP2A2水平,并增加细胞内钙浓度,而抑制则产生相反的效果。miR-328可能参与亚硒酸钠对H9c2细胞中H₂O₂诱导的细胞死亡的作用。