Propofol attenuates the production of lipopolysaccharide (LPS)-stimulated proinflammatory mediators and microglia-mediated neurotoxicity in vitro. (A–E) Propofol pretreatment dose dependently attenuated LPS-induced production of (A) nitric oxide (NO), (B) reactive oxygen species (ROS), (C) tumor necrosis factor-α (TNF-α), (D) interlukin (IL)-1β, and (E) cell proliferation in primary rat microglial cells. N = 6 independent measurements. (F) Conditioned medium from LPS-stimulated microglia induced increased release of lactate dehydrogenase (LDH) in embryonic cortical neuronal. Pretreatment of microglia with propofol before LPS stimulation and addition of conditioned media to neurons resulted in reduced cell death. N = 6 independent measurements. (G–I) LPS stimulation also increased Iba-1 and inducible NO synthase (iNOS) expression in primary cortical microglia, and propofol pretreatment significantly reduced Iba-1 and iNOS expression after 24 h. N = 4 independent measurements. #P < 0.05, ###P < 0.001 versus control; *P < 0.05, **P < 0.01, ***P < 0.001 versus LPS group. Statistical analyses were performed by one-way ANOVA with Student–Newman–Keuls post hoc test. GAPDH = glyceraldehyde-3-phosphate dehydrogenase; Iba-1 = ionized calcium-binding adapter molecule 1.