Skip to main content
. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: Front Neuroendocrinol. 2011 Nov 4;33(1):85–104. doi: 10.1016/j.yfrne.2011.10.001

Figure 5. E2 attenuates NADPH oxidase activity, superoxide production and oxidative damage in hippocampal CA1 after global cerebral ischemia.

Figure 5

(A) Time course of NADPH oxidase activity (a) and superoxide production (b) in hippocampal CA1 region from sham, placebo (Pla) and E2-treated rats. Values are means ±SE of 4–5 rats in each group and expressed as fold changed vs. sham+Pla group. *P < 0.05 vs. sham; #P < 0.05 vs. Pla at the same time point. There was no difference between Pla+sham and E2+sham groups. (B) Effects of ICI182,780 on NADPH oxidase activity (a) and superoxide production (b) in CA1 at 3h after reperfusion. *P < 0.05 vs. vehicle group. (C) Representative pictures of oxidized HEt staining taken from medial CA1 region 3 h after reperfusion. Strong oxidized HEt staining was detected in Pla and E2+ICI treated brains after ischemia, while weak oxidized HEt signals were detected in sham and E2 groups (a). E2 significantly attenuated superoxide generation compared to Pla, which was reversed by ICI182,780 (b). *P < 0.01, vs. sham and E2. (D) Effect of E2 on oxidative damage markers for lipid peroxidation (4-HNE) and DNA damage (8-OHdG) 1 day after ischemia. Note that E2 strongly decreased 4-HNE and 8-OHdG staining. Scale bar in all sections = 50 μm; Magnification, 40×. HEt: hydroethidine; ICI: ICI182,780. Adapted from [203].

HHS Vulnerability Disclosure