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microRNA-454 通过靶向 NADPH 氧化酶 4（NOX4）调节脑缺血/再灌注损伤后的氧化应激和神经元细胞凋亡。

MicroRNA-454 modulates the oxidative stress and neuronal apoptosis after cerebral ischemia/reperfusion injury via targeting NADPH oxidase 4 (NOX4).

机构信息

Department of Neurology, Baoan District Central Hospital, Shenzhen City, Guangdong Province, P.R. China.

Department of Neurology, Ningxia Hui Autonomous Region People's Hospital, Yinchuan City, Ningxia Hui Autonomous Region, P.R. China.

出版信息

J Biochem Mol Toxicol. 2022 Oct;36(10):e23153. doi: 10.1002/jbt.23153. Epub 2022 Aug 31.

DOI:10.1002/jbt.23153
PMID:36043333
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9786265/
Abstract

To investigate the function of miR-454 in ischemic stroke, this study was carried out. Cerebral ischemia/reperfusion (I/R) injury animal model and a SHSY5Y cell culture model of oxygen-glucose deprivation/reoxygenation (OGD/R) were constructed. The effects of miR-454 were detected by evaluating the levels of biochemical markers, gene expression, and pathophysiological markers. The results showed that NOX4 level was elevated, while miR-454 expression was reduced in I/R brain samples and in OGD/R-treated cells. The miR-454 agomir declined NOX4 level and reactive oxygen species (ROS) production in rats suffering from I/R. Furthermore, microRNA-145 (miR-454) overexpression inhibited NOX4 level and ROS production in cells treated by OGD/R and decreased luciferase activity in cells transfected with NOX4-wild type (WT) reporter plasmid. Meanwhile, our results proved that the protected effects of miR-454 on SH-SY5Y cells treated by OGD/R were reversed by pcDNA-NOX4 transfection. MiR-454 protected animals from brain injury induced by cerebral I/R via directly regulating its target gene NOX4, illustrating a curatively potential target for treating ischemic stroke.

摘要

为了研究 miR-454 在缺血性脑卒中中的作用，本研究进行了一系列实验。构建了脑缺血/再灌注（I/R）损伤动物模型和氧葡萄糖剥夺/复氧（OGD/R）的 SH-SY5Y 细胞培养模型。通过评估生化标志物、基因表达和病理生理标志物的水平来检测 miR-454 的作用。结果表明，在 I/R 脑样本和 OGD/R 处理的细胞中，NOX4 水平升高，而 miR-454 表达降低。在 I/R 大鼠中，miR-454 激动剂降低了 NOX4 水平和活性氧（ROS）的产生。此外，miR-454 过表达抑制了 OGD/R 处理的细胞中 NOX4 水平和 ROS 的产生，并降低了转染 NOX4 野生型（WT）报告质粒的细胞中的荧光素酶活性。同时，我们的结果证明，miR-454 对 OGD/R 处理的 SH-SY5Y 细胞的保护作用可被 pcDNA-NOX4 转染逆转。miR-454 通过直接调节其靶基因 NOX4 来保护动物免受脑 I/R 引起的脑损伤，这为治疗缺血性脑卒中提供了潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/59f7d8e5c240/JBT-36-e23153-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/1cd6fec1a497/JBT-36-e23153-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/59f7d8e5c240/JBT-36-e23153-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/1cd6fec1a497/JBT-36-e23153-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/543f830ac5f6/JBT-36-e23153-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c6e/9786265/59f7d8e5c240/JBT-36-e23153-g008.jpg

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