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- Title
Inhibition of miR-145-5p Reduces Spinal Cord Injury-Induced Inflammatory and Oxidative Stress Responses via Affecting Nurr1-TNF-α Signaling Axis.
- Authors
Jiang, Lei; Wei, Zeng-Chun; Xu, Li-Li; Yu, Shan-Ying; Li, Chao
- Abstract
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.
- Subjects
OXIDATIVE stress; SPINAL cord; ENZYME-linked immunosorbent assay; SPRAGUE Dawley rats; ANIMAL disease models
- Publication
Cell Biochemistry & Biophysics, 2021, Vol 79, Issue 4, p791
- ISSN
1085-9195
- Publication type
Article
- DOI
10.1007/s12013-021-00992-z