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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: A possible role of microglia-derived nitric oxide by lipopolysaccharide in activation of astroglial pentose-phosphate pathway via the Keap1/Nrf2 system

Fig. 4

The effects of U0126-pretreatment on microglia and astroglia. U0126 pretreatment eliminated LPS-induced production of NO in untreated astroglia and in microglia. The rate of ROS production (a ROS) and the rate of NO production (b NO) in the astroglial culture exposed to LPS (0.01 μg/mL) for 12 h in the presence or absence of U0126 (10 μmol/L). Cells had been incubated with U0126 for 12 h before exposure to LPS. Values are the mean ± SD of six wells. n.s., not significant, **P < 0.01, ***P < 0.001 versus control (grouped t test). The rate of ROS production (c ROS), and the rate of NO production (d NO) in the microglial culture exposed to LPS (0.01 μg/mL) for 12 h in the presence or absence of U0126 (10 μmol/L). Basal production of ROS and NO in astroglia or microglia was assessed with or without pretreatment of U0126 for 24 h. ROS production was reduced by U0126 in microglia, while astroglial ROS production was not affected (e ROS). Neither astroglial nor microglial NO production was altered by U0126 pretreatment (f NO). Values are the mean ± SD of four wells. n.s., not significant, *P < 0.05, **P < 0.01 versus control (grouped t test)

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