Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase
J. Clin. Invest. Sang Won Suh, et al. 117:910 doi:10.1172/JCI30077 [Go to this article.]

Figure 3
Inhibition of NADPH oxidase prevents HG-induced neuronal death. (A) GD/GR-induced superoxide production in cortical neurons is attenuated by p47^phox deficiency. Data are mean + SEM; n = 3; *P < 0.05 versus WT. (B) GD/GR-induced neuronal death is blocked by p47^phox gene deletion and by pharmacological inhibitors of NADPH oxidase activity. Photomicrographs show propidium iodide (PI) staining of dead neurons 22 hours after GD in WT neurons, p47^phox-deficient neurons, or WT neurons treated with 6-aminonicotinamide or apocynin. Scale bar: 100 μm. Data are mean + SEM; n = 4–6; *P < 0.05. (C) Photomicrographs show dead neurons stained green by Fluoro-Jade B in the hippocampal CA1 region of WT and p47^phox-deficient mice 7 days after HG/GR. Graph quantifies hypoglycemic neuronal death in 4 vulnerable brain regions. Scale bar: 100 μm; data are mean + SEM; n = 3; *P < 0.05. (D) HG/GR-induced superoxide production, as evidence by Et fluorescence, was attenuated in neurons of p47^phox-deficient mice. Scale bar: 100 μm; data are mean + SEM; n = 3–4; *P < 0.05. (E) Apocynin reduced neuronal death in WT rats evaluated 7 days after HG/GR. Data are mean + SEM; n = 5; *P < 0.05.