Fig. 6.
Propofol dose dependently attenuates lipopolysaccharide (LPS)-stimulated release of proinflammatory mediators in BV2 microglial cells. LPS stimulation induced significant increases in the production of (A) nitric oxide (NO), (B) reactive oxygen species (ROS), and (C) tumor necrosis factor-α (TNF-α) in BV2 cells, whereas propofol pretreatment significantly attenuated LPS-stimulated NO, ROS, and TNF-α production. N = 6 independent measurements. ### P < 0.001 versus control, ** P < 0.01. ***P < 0.001 versus LPS group. Statistical analyses were performed by one-way ANOVA with Student–Newman–Keuls post hoc test.

Propofol dose dependently attenuates lipopolysaccharide (LPS)-stimulated release of proinflammatory mediators in BV2 microglial cells. LPS stimulation induced significant increases in the production of (A) nitric oxide (NO), (B) reactive oxygen species (ROS), and (C) tumor necrosis factor-α (TNF-α) in BV2 cells, whereas propofol pretreatment significantly attenuated LPS-stimulated NO, ROS, and TNF-α production. N = 6 independent measurements. ### P < 0.001 versus control, ** P < 0.01. ***P < 0.001 versus LPS group. Statistical analyses were performed by one-way ANOVA with Student–Newman–Keuls post hoc test.

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