Abstract: Objective To investigate the effect of propofol on inflammatory cytokines activation by regulating the nuclear factor kappa-B ( NF-κB ) signaling pathway in BV2 microglial cells. Methods BV2 cells were divided into 5 groups: control group, model group, propofol low-dose group (20 μmol / L), propofol medium-dose group (50 μmol / L), and propofol high-dose group (100 μmol / L). Cell viability was detected by CCK-8 assay. The levels of interleukin-6 (IL6), IL-1β, tumor necrosis factor-α ( TNF-α), nitric oxide synthase (NOS) were detected by ELISA, and the reactive oxygen species (ROS) was detected by ROS assay kit. Western blotting analysis was used to detect the expression levels of NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD ( ASC), Caspase-1, IκB, P65, and p-P65. Immunofluorescence staining was used to observe the nuclear translocation of P65. Results Propofol showed no toxicity to BV3 cells for all three concentrations. The levels of IL-6, IL-1β, TNF-α, ROS, and NOS in the LPS group were significantly increased when compared with those in the control group (P< 0. 01). The expression of IκB was significantly down-regulated, p-P65 / P65 was significantly up-regulated, and P65 nuclear translocation was significantly increased ( P < 0. 01). After treatment with different doses of propofol, the results of above indexes were reversed, IL-6, IL-1β, TNF-α, ROS and NOS levels were significantly reduced (P < 0. 01), the expression of IκB was significantly up-regulated, p-P65 / P65 was significantly down-regulated, and nuclear localized p65 protein was significantly reduced (P< 0. 01). All changes in the above results were dose-dependent. Conclusion Propofol alleviate the activation of inflammatory cytokines in LPS stimulated BV2 cells by regulating the NF-κB signaling pathway. 

Key words: propofol, NF-κB, inflammatory cytokines, BV2 cells