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. 2010 Sep 22;31(3):868–880. doi: 10.1038/jcbfm.2010.166

Figure 6.

Figure 6

Nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase (NOX) inhibition alleviated microglial activation and medium spiny neuron (MSN) injury. (A) Representative photomicrographs of Iba-1 staining of the striatum 72 hours after transient global cerebral ischemia (tGCI). Microglial activation was suppressed by NOX inhibition. (B) Representative photomicrographs of the striatum 72 hours after tGCI. Sections were stained with cresyl violet, terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end labeling (TUNEL), and a DARPP-32 antibody. Scale bars=100 μm. (C) Cell counting study showed a significant decrease in TUNEL-positive cells in the gp91 knockout (KO) and apocynin-treated mice compared with the wild-type (WT) and vehicle-treated mice (n=5, *P<0.05). (D) Apoptosis-related DNA fragmentation assay. In the WT mice, DNA fragmentation increased significantly in the striatum 72 hours after tGCI compared with the sham animals (n=5, *P<0.01). (E) DNA fragmentation in the gp91 KO and apocynin-treated mice 72 hours after tGCI decreased significantly compared with the WT and vehicle-treated mice (n=6, *P<0.05). Apo, apocynin; Veh, vehicle.