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. 2012 Jun 8;287(32):27189–27203. doi: 10.1074/jbc.M112.346932

FIGURE 3.

FIGURE 3.

Activation of PI3K and AKT by gemfibrozil in microglia. A, mouse BV-2 microglial cells were treated with 50 μm gemfibrozil (Gem) under serum-free conditions for different minutes followed by analysis of the recruitment of p110α (panel i), p110β (panel ii), and p110γ (panel iii) to the cellular membrane via Western blot. TLR2 was used as a loading control for membrane fragments. B, densitometric analysis of dose-dependent change (relative to TLR2) of PI3K subunits by gemfibrozil treatment. C, BV-2 cells were treated with 50 μm gemfibrozil for different minutes followed by monitoring the activation of AKT by Western blot with antibodies against phospho-AKT and total AKT. D, densitometric analysis of dose-dependent change (relative to TLR2) of PI3K subunits by gemfibrozil treatment. Mouse primary microglia were treated with 50 μm gemfibrozil for different minutes followed by double-labeling for CD11b and either phospho-AKT (E) or total AKT (F). DAPI was used to stain nuclei. Results are means ± S.D. of at least three independent experiments. a, p < 0.001 versus control. Scale bar, 20 μm. UN, untreated.