下调和上调
免疫印迹
活力测定
细胞凋亡
医学
MTT法
再灌注损伤
化学
细胞
缺血
分子生物学
细胞生物学
癌症研究
生物
基因
生物化学
内科学
作者
B Liu,Tangbing Xu,Ying Meng
出处
期刊:PubMed
日期:2020-04-24
卷期号:34 (2)
被引量:4
摘要
Many lncRNAs have been reported to affect cerebral ischemia/reperfusion (I/R) injury. The purpose of this study is to elucidate the role of lncRNA NEAT1 as well as the regulatory mechanism of lncRNA NEAT1/miR-874-3p in cerebral I/R injury. A cellular model of cerebral I/R injury was built. RT-qPCR was used to detect NEAT1 and miR-874-3p expression. Cell viability was detected by MTT assay. The expression of apoptosis-related proteins (Bcl-2 and Bax) was measured by Western blot analysis. The relationship between NEAT1 and miR-874-3p was confirmed by dual luciferase reporter assay. We found that LncRNA NEAT1 was upregulated in the PC12 cells treated by I/R and upregulation of lncRNA NEAT1 can aggravate I/R injury of PC12 cells. Additionally, lncRNA NEAT1 overexpression decreased cell viability and induced apoptosis in PC12 cells treated by I/R. Furthermore, miR-874-3p was confirmed to be a target of lncRNA NEAT1. mR-874-3p and NEAT1 expression are found to be reciprocally inhibited in PC12 cells. In summary, LncRNA NEAT1 aggravates cerebral I/R injury by suppressing miR-874-3p expression.
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