Rosiglitazone Ameliorates Spinal Cord Injury via Inhibiting Mitophagy and Inflammation of Neural Stem Cells

Figure 5

Effects of the forced FOXO1 expression on cell proliferation, mitochondrial OXPHOS, and glycolysis. (a–d) Effects of the forced FOXO1 expression on cell proliferation reflected by CCK-8 measurements (a), ATP production (b), and Edu staining (c, d). The proportions of cell proliferation among four groups were statistically analyzed. DAPI (blue) and Edu (green) represent the nucleus and the newly synthesized DNA, respectively. (e, f) Effects of FOXO1 expression on state 3 respiration in the absence (e) or presence (f) of fatty acid. (g) Ratios of Cox I or IV/VDAC1 were determined by densitometric analysis. Representative immunoblots of Cox I and Cox IV under the forced FOXO1 expression by DOX. VDAC1 served as the loading control. (h) Effect of Rosi on ATP level produced by glycolysis. FOXO1 was induced by DOX to the level similar to that without Rosi. Data represent three independent experiments and are expressed as (a–c, e–h). versus Rosi+PBS; ^# versus DMSO. FA: fatty acid.

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