Fig. 4. HO2 treatment increased oxidative stress in the hippocampus of mice. (A~C) Experimental design (A). Mice were treated with HO2 (100% O2) at 2.0 ATA for 1 h. Red arrow, time point for tissue preparation. Photomicrographs showing DHE-reactive oxidative stress in the hippocampus (B) of normal mice exposed to 1-h hyperoxygenation and quantification levels (C). Scale bar; 400 µm. n=8 animals per group. (D~F) Experimental design (D). Wild-type mice (WT) or Ncf1 knockout mice (Ncf1-/-) were treated with HO2 (100% O2) at 2.0 ATA for 1 h daily for 7 days. Red arrow, time point for tissue preparation. Photomicrographs showing DHE-reactive oxidative stress in the hippocampus of wild-type mice or Ncf1 KO mice exposed to 7 days of HO2 (D) and their quantification levels (E). Scale bar; 400 µm. n=8~10 animals per group. (G~I) Experimental design (G). CRST mice were treated with the 14-day HO2 treatment with 100% O2 at 2.0 ATA or with imipramine (IMI; 20 mg/kg/day, i.p.) for 14 days. Red arrow, time point for tissue preparation. Photomicrographs showing DHE-reactive oxidative stress in the hippocampus of mice treated with the 14 days of HO2 or IMI injection (H) and their quantification levels (I). Scale bar; 400 µm. n=4~6 animals per group. Mean±SEM. *,**difference between indicated group. *p<0.05, **p<0.01 (Student t-test; one-way ANOVA and Newman-Keuls post hoc test; two-way ANOVA and Bonferroni post hoc test).
© Exp Neurobiol
