• Zhiwu Wu, Zhixiong Zhang, Zhihua Wang, Huaxin Zhu, and Meihua Li.
• Department of Neurosurgery＆Jiangxi Key Laboratory of Neurosurgery, The First Affiliated Hospital Of Nanchang University, Nanchang, Jiangxi, PR China.
• World Neurosurg. 2022 Jun 1; 162: e427e435e427-e435.

ObjectiveNeuroinflammation triggers sequelae after spinal cord injury (SCI). Inhibition of inflammation promotes recovery after SCI. MicroRNAs regulate many pathophysiological processes, including inflammation. Any role for miR-181a-5p in the inflammatory response after SCI remains unclear. Thus, we evaluated the effects of miR-181a-5p on inflammation in PC12 cells and the underlying mechanism in play.MethodsQuantitative reverse transcription-polymerase chain reaction was used to measure the levels of miR-181a-5p and high-mobility group box-1 protein (HMGB1) in SCI tissues. Cell-counting kit-8 assays were used to assess the viability of PC12 cells treated with lipopolysaccharide (LPS). Plasmids encoding MiR-181a-5p mimics, an miR-181a-5p inhibitor, or/and the HMGB1 were transfected into PC12 cells. Quantitative reverse transcription-polymerase chain reaction or/and Western blotting were performed to assess the expression of miR-181a-5p, HMGB1, and inflammatory factors in vitro.ResultsMiR-181a-5p expression decreased and HMGB1 expression increased in SCI tissues and LPS-induced PC12 cells. Upregulation of miR-181a-5p (via transfection) inhibited inflammation of, and HMGB1 expression by, LPS-induced PC12 cells. HMGB1 overexpression reversed the anti-inflammatory effects of miR-181a-5p. Dual-luciferase assays confirmed that HMGB1 was a direct target of miR-181a-5p.ConclusionsmiR-181a-5p attenuated the inflammatory response of LPS-induced PC12 cells by directly inhibiting HMGB1; thus, miR-181a-5p may serve as a therapeutic target in SCI.Copyright © 2022 Elsevier Inc. All rights reserved.

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