Glutathione Suppresses Cerebral Infarct Volume and Cell Death after Ischemic Injury: Involvement of FOXO3 Inactivation and Bcl2 Expression

Figure 6

The immunocytochemical image to evaluate the activation of FOXO3 in H/R injured bEnd.3 cells. (a) The activation of FOXO3 was evaluated with immunocytochemistry. This image showed the translocation of FOXO3 to the nucleus of b.END3 cells in the H/R group was increased compared with the normal control group. 1 mM GSH pretreatment group with H/R injury group showed suppression of FOXO3 translocation to the nucleus compared with the hypoxia group. 1 mM GSH decreased the activation of FOXO3 under hypoxic condition. (b) This ortho image shows the activation of FOXO3 by suggesting the translocation of FOXO3 into the nucleus. The translocation of FOXO3 into the nucleus was evidently showed in the H/R group whereas the translocation of FOXO3 into the nucleus was reduced by treating GSH in spite of the H/R stress. Each experiment included 3 repeats per condition. Scale bar = 400 μm, H/R: hypoxia 6 hr, and reperfusion 18 hr injury group, GSH + H/R: GSH pretreatment and hypoxia 6 hr and reperfusion 18 hr injury group.

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