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Knocking Down KCNQ1OT1 Suppressed LPS-Induced Neuroinflammation and Neuronal Apoptosis in HMC3 Cells For further exploring the function of KCNQ1OT1, we transfected HMC3 cells with pc-KCNQ1OT1 or si-KCNQ1OT1. The expression of KCNQ1OT1 was evaluated by RT-qPCR. Compared with control cells (cells transfected with pc-NC or si-NC), the expression of KCNQ1OT1 in HMC3 cells transfected with pc-KCNQ1OT1 was significantly increased, while the expression of KCNQ1OT1 in cells transfected with si-KCNQ1OT1 was significantly decreased (Figure 2A). Subsequently, we used RT-qPCR and ELISA kits to examine the expressions of TNF-α, IL-1β and IL-6 to evaluate the inflammatory response. The results indicated that LPS treatment markedly promoted the expression levels of inflammatory cytokines TNF-α, IL-1β and IL-6 in HMC3 cells; overexpression of KCNQ1OT1 promoted the expressions of inflammatory cytokines, while KCNQ1OT1 knockdown inhibited their expression (Figure 2B and C). The expression of M1 p

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