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Aixia Song,1 Yuying Yang,2 Hongmei He,1 Jian Sun,1 Qing Chang,1 Qian Xue1 1Department of Neurology, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of China; 2Stroke Office, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaCorrespondence: Qian XueDepartment of Neurology, The First Affiliated Hospital of Hebei North University, No. 12 Changqing Road, Qiaoxi District, Zhangjiakou, Hebei, 075000, People’s Republic of ChinaEmail qianyanxin7@163.comBackground: Neuroinflammation and neuronal apoptosis are considered as the critical factors in the pathogenesis of multiple neurological diseases. Recent studies have shown that long non-coding RNA (lncRNA) plays a crucial part in neuroinflammation and neuronal apoptosis.Methods: The expression levels of lncRNA KCNQ1OT1, miR-30e-3p and NLRP3 in lipopolysaccharide (LPS)-induced HMC3 cells were analyzed using RT-qPCR. MTT assay, LDH release assay and ELISA were used to assess the effect of KCNQ1OT1 and miR-30e-3p on neuroinflammation and neuronal apoptosis. The targeted regulatory relationships among KCNQ1OT1, miR-30e-3p and NLRP3 were evaluated by bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR and Western blot.Results: In LPS-induced HMC3 cells, the expression levels of KCNQ1OT1 and NLRP3 were increased, while the expression level of miR-30e-3p was reduced. Knockdown of KCNQ1OT1 alleviated LPS-induced apoptosis and neuroinflammation of HMC3 cells, accompanied by increased cell viability, low LDH release and reduced cell apoptosis rate, and reduced levels of TNF-α, IL-1β and IL-6. Overexpression of miR-30e-3p had a similar effect. Additionally, KCNQ1OT1 could bind with miR-30e-3p and repress its expression in HMC3 cells, and KCNQ1OT1 overexpression counteracted miR-30e-3p’s inhibitory effect on LPS-induced neuronal damage and inflammatory response in HMC3 cells. Furthermore, KCNQ1OT1 could positively regulate the expression of NLRP3 via repressing miR-30e-3p.Conclusion: Inhibition of KCNQ1OT1 could reduce neuroinflammation and neuronal apoptosis induced by LPS in HMC3 cells by regulating miR-30e-3p/NLRP3 pathway, suggesting that KCNQ1OT1 and miR-30e-3p could serve as promising therapeutic targets for treating neurological diseases.Keywords: NLRP3, KCNQ1OT1, miR-30e-3p, neuroinflammation