Knockdown of lncRNA SNHG14 alleviates LPS-induced inflammation and apoptosis of PC12 cells by regulating miR-181b-5p
- Hui Jiang
- Jie Ni
- Yan Zheng
- Yun Xu
Affiliations: Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China, Department of Emergency, Affiliated Drum Tower Hospital of Nanjing University, Nanjing, Jiangsu 210000, P.R. China, Department of Neurology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- Published online on: March 17, 2021 https://doi.org/10.3892/etm.2021.9928
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Spinal cord injury (SCI) is a traumatic central nervous system disorder that leads to permanent functional loss, and unavailable treatment of this disease results in poor quality of life. However, the specific role of long non-coding RNA small nucleolar RNA host gene 14 (lncRNA SNHG14) in SCI has not been fully studied. The aim of the current study was to investigate the role of SNHG14 and its regulatory mechanism in lipopolysaccharide (LPS)-induced PC-12 cells. LPS was used to stimulate PC-12 cells to simulate inflammatory injury following SCI in vitro. Cell viability and apoptosis were respectively assessed by Cell Counting Kit-8 assay and TUNEL assay. Western blotting was performed to detect the expressions of apoptosis-related proteins. The mRNA levels of SNHG14 and microRNA (miR)-181b-5p were detected by reverse transcription-quantitative PCR. The target of SNGH14 was predicted by bioinformatics analysis and subsequently validated by a luciferase reporter assay. ELISA was then used to detect the levels of inflammatory factors. The results indicated that LPS induced inflammation, decreased cell viability and increased the apoptosis of PC-12 cells. Interference of SNHG14 alleviated this type of injury of PC-12 cells. Bioinformatics prediction and luciferase reporter assay demonstrated that miR-181b-5p could directly bind to SNHG14. Moreover, mechanistic investigations revealed that the miR-181b-5p inhibitor could reverse the inhibitory effects of SNHG14 silencing on cell viability, inflammation and apoptosis of PC-12 cells. To conclude, the present results showed that SNHG14 knockdown alleviated PC-12 cell inflammation and apoptosis induced by LPS via regulating miR-181b-5p, which might provide a novel insight into the treatment of SCI.