Figure 7.

Evidence that ERα mediates E₂-induced attenuation of NADPH activity and superoxide production as well as E₂-induced neuroprotection in hippocampal CA1 region after ischemia. A, Alexa488N-MS-ODNs (10 nmol) were bilaterally infused into the lateral ventricles, and 3 h later the brains were fixed, sectioned, and subjected to label with NeuN (red). Images were then visualized under confocal microscopy. Note that fluorescent MS was distributed in cytoplasm and predominantly in the dorsal hippocampal CA1 subregion. B, Western blot analysis demonstrates a robust reduction in ERα or ERβ expression after pretreatment with ERα or ERβ AS-ODNs compared with MS-ODNs controls or sham controls (a, b). *p < 0.05 versus MS treatment group, respectively. C, Effects of ERα or ERβ AS on E₂ attenuation of NADPH oxidase activity and superoxide production in CA1 region at 3 h reperfusion. *p < 0.05 versus E₂ + MS group; ^†p > 0.05 versus E₂ + MS group. D, Effect of MS, ERα, or ERβ AS on E₂ neuroprotection against cerebral ischemia. Representative CA1 sections double stained with NeuN (red) and Fluoro-Jade B (green) from E₂-treated animals with ERα AS, ERβ AS, or MS infusion. Note that E₂ protection was abolished only in the ERα AS-infused rat hippocampus (a). Values are means ± SE from six to seven animals (b). *p < 0.05 versus E₂ + MS group. Scale bars, 50 μm. Magnification, 40×. n.s., No significant difference.