Skip to main content
. 2022 Feb 28;49(4):55. doi: 10.3892/ijmm.2022.5111

Figure 5.

Figure 5

(A and B) HIF-1α immunohistochemistry in CA1 of the (A) NT/sham (a-c), (B) NT/ischemia (a-g), (A) HT/sham (d-f) and (B) HT/ischemia (h-n) groups at 0, 3, 6 and 12 h, 1, 2 and 5 days after TFI. In the NT/sham group, HIF-1α immunoreactivity in the SP was very weak. In the NT/ischemia group, HIF-1α immunoreactivity in the SP was significantly increased at 12 h and 1 day (asterisk), markedly reduced at 2 days and again increased at 5 days after TFI. In the HT/sham group, HIF-1α immunoreactivity was very high (asterisk) at 0 h and similar to that of the NT/sham group from 3 h after sham TFI. In the HT/ischemia group, increased HIF-1α immunoreactivity was gradually increased until 12 h after TFI and thereafter was lower (asterisk) than that in the HT/sham group. Scale bar, 50 µm. (C) Relative optical density (ROD) (% of NT/sham group) of HIF-1α immunoreactivity in CA1. *P<0.05 vs. NT/sham group at 0 h; †P<0.05 vs. pre-time point group; #P<0.05 vs. NT/ischemia group. The bars indicate the means ± SEM (n=7, respectively). HIF-1α, hypoxia-inducible factor 1α; NT, normothermia; HT, hyperthermia; TFI, transient forebrain ischemia.