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 [
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Figure 1GR induces neuronal superoxide production after HG. (
A) Neuronal superoxide production as imaged by Et fluorescence in rat brain hippocampal sections after sham HG (Sham), 60 minutes of HG without GR (HG only), or 30 minutes of HG plus 30 minutes of GR (HG/GR). Et signal intensity is expressed as the ratio of the mean fluorescence in neuronal perikarya (example outlined in white dashed line) to background (stratum radiatum; white square). Scale bar: 100 μm. Data are mean + SEM;
n = 4; *
P < 0.05; **
P < 0.01. (
B) Et fluorescence induced by HG/GR was blocked by tempol and by overexpression of SOD-1 (SOD-1 Tg). Data are mean + SEM;
n = 3–5; *
P < 0.05. (
C) Tempol and SOD-1 overexpression also reduced neuronal death after HG/GR. H&E-stained sections of the hippocampal CA1 cell layer prepared 7 days after HG/GR show degenerating neurons with pyknotic, eosinophilic changes (arrows). Scale bar: 100 μm. (
D) The number of degenerating neurons was quantified in 4 brain regions: hippocampal CA1, subiculum (Sub), dentate gyrus (DG), and perirhinal cortex (Ctx). Data are mean + SEM;
n = 7–10; *
P < 0.05 versus HG/GR alone in each region.
