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Inhibition of miR-145-5p Reduces Spinal Cord Injury-Induced Inflammatory and Oxidative Stress Responses via Affecting Nurr1-TNF-α Signaling Axis
Cell Biochemistry and Biophysics ( IF 2.6 ) Pub Date : 2021-06-16 , DOI: 10.1007/s12013-021-00992-z
Lei Jiang 1 , Zeng-Chun Wei 2 , Li-Li Xu 3 , Shan-Ying Yu 4 , Chao Li 5
Affiliation  

Inflammation and oxidative stress feature prominently in the secondary spinal cord injury (SCI). The present work is targeted at deciphering miR-145-5p’s role and underlying mechanism in SCI. We randomly divided Sprague-Dawley rats into SCI group and control group. Microglial BV2 cells were separated into control group and lipopolysaccharide (LPS) treatment group. Enzyme-linked immunosorbent assay was carried out for determining the concentrations of interleukin-6, interleukin-1β, and tumor necrosis factor-α (TNF-α). The expressions of malondialdehyde, glutathione peroxidase, superoxide dismutase, and reactive oxygen species were also detected. TNF-α, miR-145-5p, and Nurr1 expressions were examined by western blot and quantitative real-time polymerase chain reaction. Western blotting and dual-luciferase reporter gene assay were conducted to examine the regulating impact that miR-145-5p had on Nurr1 and TNF-α. MiR-145-5p was remarkably upregulated in the SCI rat model’s spinal cord tissues and BV2 cells treated with LPS, and Nurr1 expression was dramatically lowered. Furthermore, miR-145-5p inhibition markedly repressed inflammatory and oxidative stress responses. Moreover, it was proved that Nurr1 was a direct miR-145-5p target. The inhibition of miR-145-5p helped promote Nurr1 expression to block TNF-α signaling. MiR-145-5p inhibition mitigates inflammation and oxidative stress via targeting Nurr1 to regulate TNF-α signaling, which ameliorates SCI.



中文翻译:

抑制 miR-145-5p 通过影响 Nurr1-TNF-α 信号轴减少脊髓损伤引起的炎症和氧化应激反应

炎症和氧化应激在继发性脊髓损伤 (SCI) 中表现突出。目前的工作旨在破译 miR-145-5p 在 SCI 中的作用和潜在机制。我们将 Sprague-Dawley 大鼠随机分为 SCI 组和对照组。将小胶质细胞BV2细胞分为对照组和脂多糖(LPS)处理组。进行酶联免疫吸附测定以确定白细胞介素6、白细胞介素1β和肿瘤坏死因子-α(TNF-α)的浓度。还检测了丙二醛、谷胱甘肽过氧化物酶、超氧化物歧化酶和活性氧的表达。通过蛋白质印迹和定量实时聚合酶链反应检查 TNF-α、miR-145-5p 和 Nurr1 的表达。进行蛋白质印迹和双荧光素酶报告基因测定以检查miR-145-5p对Nurr1和TNF-α的调节影响。在 SCI 大鼠模型的脊髓组织和 LPS 处理的 BV2 细胞中,MiR-145-5p 显着上调,Nurr1 表达显着降低。此外,miR-145-5p 抑制显着抑制炎症和氧化应激反应。此外,证明Nurr1是直接的miR-145-5p靶标。抑制 miR-145-5p 有助于促进 Nurr1 表达以阻断 TNF-α 信号传导。MiR-145-5p 抑制通过靶向 Nurr1 来调节 TNF-α 信号传导来减轻炎症和氧化应激,从而改善 SCI。在 SCI 大鼠模型的脊髓组织和 LPS 处理的 BV2 细胞中,MiR-145-5p 显着上调,Nurr1 表达显着降低。此外,miR-145-5p 抑制显着抑制炎症和氧化应激反应。此外,证明Nurr1是直接的miR-145-5p靶标。抑制 miR-145-5p 有助于促进 Nurr1 表达以阻断 TNF-α 信号传导。MiR-145-5p 抑制通过靶向 Nurr1 来调节 TNF-α 信号传导来减轻炎症和氧化应激,从而改善 SCI。在 SCI 大鼠模型的脊髓组织和 LPS 处理的 BV2 细胞中,MiR-145-5p 显着上调,Nurr1 表达显着降低。此外,miR-145-5p 抑制显着抑制炎症和氧化应激反应。此外,证明Nurr1是直接的miR-145-5p靶标。抑制 miR-145-5p 有助于促进 Nurr1 表达以阻断 TNF-α 信号传导。MiR-145-5p 抑制通过靶向 Nurr1 来调节 TNF-α 信号传导来减轻炎症和氧化应激,从而改善 SCI。抑制 miR-145-5p 有助于促进 Nurr1 表达以阻断 TNF-α 信号传导。MiR-145-5p 抑制通过靶向 Nurr1 来调节 TNF-α 信号传导来减轻炎症和氧化应激,从而改善 SCI。抑制 miR-145-5p 有助于促进 Nurr1 表达以阻断 TNF-α 信号传导。MiR-145-5p 抑制通过靶向 Nurr1 来调节 TNF-α 信号传导来减轻炎症和氧化应激,从而改善 SCI。

更新日期:2021-06-17
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