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首页> 外文期刊>Artificial cells, nanomedicine, and biotechnology. >Knockdown of lncRNA Gm11974 protect against cerebral ischemic reperfusion through miR-766-3p/NR3C2 axis
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Knockdown of lncRNA Gm11974 protect against cerebral ischemic reperfusion through miR-766-3p/NR3C2 axis

机译:敲低lncRNA Gm11974通过miR-766-3p / NR3C2轴防止脑缺血再灌注

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Aims: In previous studies, numerous differential lncRNAs in cerebral ischemic reperfusion injury were identified using RNA-Seq analysis. However, little is known about whether and how lncRNAs involved in cerebral I/R injury. In this study, we investigated the function and explored the possible mechanism of lncRNA Gm11974 in cerebral I/R injury. Methods: Oxygen glucose deprivation model in N2a cells were utilized to mimic the cerebral I/R injury in vitro. Trypan blue staining, Tunel, JC-1 and cell viability were measured to evaluate the function of lncRNA Gm11974. Dual-luciferase reporter assay was used to explore the potential mechanism of lncRNA Gm11974. Results: Gm11974 was mainly located in cytoplasm. Knockdown of lncRNA Gm11974 alleviated the apoptosis induced by OGD and cell death rates were significantly reduced. We further provided the possible mechanism that Gm11974/miR-766-3p/NR3C2 axis plays important role in cerebral I/R injury. Conclusions: We evaluated the function and mechanism of lncRNA Gm11974 in ischemic brain injury. LncRNA Gm11974 may serve as a potential target for new therapeutic intervention.
机译:目的:在先前的研究中,使用RNA-Seq分析鉴定了脑缺血再灌注损伤中的许多差异性lncRNA。但是,对于lncRNA是否以及如何参与脑I / R损伤知之甚少。在这项研究中,我们调查了功能和lncRNA Gm11974在脑I / R损伤中的可能机制。方法:利用N2a细胞中的缺氧葡萄糖模型模拟体外脑缺血再灌注损伤。测量了台盼蓝染色,Tunel,JC-1和细胞活力,以评估lncRNA Gm11974的功能。用双重荧光素酶报告基因检测了lncRNA Gm11974的潜在机制。结果:Gm11974主要位于细胞质中。敲低lncRNA Gm11974减轻了OGD诱导的细胞凋亡,并显着降低了细胞死亡率。我们进一步提供了Gm11974 / miR-766-3p / NR3C2轴在脑I / R损伤中发挥重要作用的可能机制。结论:我们评估了lncRNA Gm11974在缺血性脑损伤中的功能和机制。 LncRNA Gm11974可能作为新的治疗手段的潜在靶标。

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