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Figure 7 | Journal of Neuroinflammation

Figure 7

From: NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration

Figure 7

Increased NOX subunit gp91 phox expression in human alcoholic brain. (A) Quantification of gp91phox + IR cells. The orbitofrontal cortex (OFC) of human postmortem alcoholic brain has a significant increase in the number of gp91phox + IR cells, compared to the OFC of human moderate drinking control brain (** P < 0.01, n = 8). (B) The representative images from the OFC of moderate drinking control brain and alcoholic brain stained with gp91phox antibody. Scale bar = 50 μm. (C) Colocalization of NOX subunit gp91phox . Brain sections from the OFC of human alcoholic brains were double-labeled for gp91phox (red) and MAP-2 (a neuronal marker), Iba1 (a microglial marker), and GFAP (an astroglial marker) (green) to analyze colabeling by using the Leica SP2 LCS confocal software. Confocal microscopy shows that gp91phox +IR cells are colocalized with MAP-2, Iba-1, and GFAP+IR cells as shown in yellow, indicating NOX subunit gp91phox is expressed in neurons (the upper panel), microglia (the middle panel) and astroglia (the lower panel). Scale bar = 10 μm. ** P < 0.01, compared with the OFC of human moderate drinking control brain.

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