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. 2009 Nov 25;29(47):14779–14789. doi: 10.1523/JNEUROSCI.4161-09.2009

Figure 6.

Figure 6.

Inhibition by TBCA and loss of CK2 by CK2-specific siRNA facilitated ROS production after ischemic stress. A, ROS production was assessed by HEt staining (red) using slices from the brains of sham, vehicle-injected, or TBCA-injected mice 1 h after ischemic reperfusion injury. DAPI (blue) was used to stain the nucleus. Scale bar, 50 μm. B, Protein nitrosylation 1 and 3 h after ischemic reperfusion was assessed by Western blot with an anti-3-NT antibody using samples from the brains of vehicle- or TBCA-injected mice. β-Tubulin was used as a loading control. C, A summary graph showing the level of 3-NT in the brains (#,##p < 0.05 compared with vehicle-I/R group; n = 6). Protein nitrosylation 1 h after OGD–reoxygenation was assessed by Western blot with an anti-3-NT antibody (D, E) using samples from CK2α siRNA or scrambled siRNA-transfected primary neuronal cells subjected to OGD and reoxygenation (#p < 0.05 compared with control; ##p < 0.05 compared with OGD and OGD/scrambled siRNA-treated groups; n = 4) or using samples from TBCA-treated primary neuronal cells subjected to OGD and reoxygenation (F, G) (#p < 0.05 compared with OGD without TBCA; n = 4 per group). I/R, Ischemic reperfusion; Mr, migration rate; O.D., optical density; R, reoxygenation; Con, control. Error bars indicate SEM.