首页> 外文期刊>Neurological Research: An Interdisciplinary Quarterly Journal >Knockdown of lncRNA SNHG1 alleviates oxygen-glucose deprivation/reperfusion-induced cell death by serving as a ceRNA for miR-424 in SH-SY5Y cells
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Knockdown of lncRNA SNHG1 alleviates oxygen-glucose deprivation/reperfusion-induced cell death by serving as a ceRNA for miR-424 in SH-SY5Y cells

机译:LNCRNA SNHG1的敲低通过用作SH-SY5Y细胞中的MIR-424的CERNA来减轻氧血糖剥夺/再灌注诱导的细胞死亡

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Objective: Long non-coding RNAs (lncRNAs) are theorized to serve a critical role in cerebral ischemia/reperfusion injury. The purpose of this study was to determine whether knockdown of lncRNA SNHG1 protected against oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell death in vitro and to investigate the underlying mechanisms. Methods: The expression levels of SNHG1 and miR-424 were detected by RT-qPCR analysis. The expression levels of apoptosis-related proteins were detected by western blot analysis. Cell viability and apoptosis were detected by MTT assay and flow cytometric analysis, respectively. Bioinformatic prediction and dual-luciferase reporter assay were performed to study the interaction between SNHG1 and miR-424. Results: The results showed that SNHG1 expression level was increased in OGD/R-treated SH-SY5Y cells, and knockdown of SNHG1 alleviates OGD/R-induced apoptosis and mitochondrial dysfunction in SH-SY5Y cells. Moreover, we found that SNHG1 might serve as a ceRNA for miR-424 in SH-SY5Y cells, and rescue experiments further confirmed that miR-424 inhibitor blocked the beneficial role of SNHG1 knockdown in OGD/R-treated SH-SY5Y cells. Conclusion: Taken together, this research supported the first evidence that lncRNA SNHG1 regulates OGD/R-induced cell death through serving as a ceRNA for miR-424 in SH-SY5Y cells.
机译:目的:广泛的非编码RNA(LNCRNA)是在脑缺血/再灌注损伤中提供关键作用的主题。本研究的目的是确定LNCRNA SNHG1的敲低是否受到氧 - 葡萄糖剥夺/再灌注(OGD / R)诱导的细胞死亡,并研究下面的机制。方法:通过RT-QPCR分析检测SNHG1和MIR-424的表达水平。通过蛋白质印迹分析检测凋亡相关蛋白的表达水平。通过MTT测定和流式细胞术分析检测细胞活力和细胞凋亡。进行生物信息预测和双荧光素酶报告结果,以研究SNHG1和MIR-424之间的相互作用。结果:结果表明,OGD / R处理的SH-SY5Y细胞中SNHG1表达水平增加,SNHG1的敲低减轻了OGD / R诱导的凋亡和SH-SY5Y细胞中的线粒体功能障碍。此外,我们发现SNHG1可以用作SH-SY5Y细胞中MIR-424的CERNA,并进一步证实MIR-424抑制剂阻断了SNHG1敲低在OGD / R处理的SH-SY5Y细胞中的有益作用。结论:携带,这项研究支持第一种证据,即LNCRNA SnHG1调节OGD / R诱导的细胞死亡,通过作为SH-SY5Y细胞中的miR-424的Cerna。

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