Fig. 1.

The effect of ginsenoside CK against neuronal bioenergy imbalance is driven by Mfn2 inactivation in the OGD/R injury model. (A) The PC12 cells were treated with oligomycin (Olig) or rotenone plus antimycin A to detect the ATP production originated from the mitochondria (mitoATP) or glycolysis (glycoATP). (B) Oxygen consumption was measured and analyzed by Seahorse XFe24 multifunctional energy metabolizer and mitochondrial pressure kit; the relative levels of oxygen consumption for basal respiration (Basal), maximal respiration consumption (MRC), spare capacity (SPC), and ATP-linked respiration (ATP) are shown on the right. (C) Glycolysis (Gly), glycolytic capacity (Gly Capacity), and glycolytic reserve (Gly Reserve) were determined by the sequential addition of 10 mM glucose (Glu), 1 μM oligomycin (Olig), or 50 mM 2-deoxy-D-glucose (2-DG) by measuring extracellular acidification rate (ECAR). (D)The expression of mitochondrial complex protein I–V was detected by western blot. β-Actin was a loading control. (E) The activities of five mitochondrial electron transfer chain enzymes were determined by enzymatic reaction kinetics kit. (F) The ratio of mitochondrial DNA/nuclear DNA was evaluated by qPCR. (G) The maximal oxygen consumption was analyzed by the LUXCEL oxygen consumption probe in the PC12 cells. Data are shown as mean ± SD, n = 3 per group; ∗P < 0.05, ∗∗P < 0.01 and ∗∗∗P < 0.001, significantly different as indicated (one-way ANOVA followed by Tukey's post hoc test).