Figure 2
Post-ischemic estradiol treatment attenuated ‘reactive gliosis’ in the ischemic area. The reactive gliosis induced after 54 h of pMCAO was measured in coronal brain sections (25 μm thick) by immunohistochemisty for GFAP and Iba1, markers of astrocytes and microglia, respectively. Representative coronal sections corresponding to the injured area (bregma −1.08) of sham-vehicle (SV), pMCAO-vehicle (IV), and pMCAO-estradiol (IE) rats are shown. The accompanying bar graph shows GFAP (A) and Iba1 (B) labeling quantified in at least 12 serial coronal sections from bregma 2.04 and −1.08 with Fiji image processing software, and expressed as the percentage of labeled tissue with respect to the total area of the photographed sections. The induction of pMCAO induced an increase in the percentage area labeled for GFAP (A) and Iba1 (B) when determined 54 h after the onset of pMCAO (IV group). Post-pMCAO estradiol treatment (IE group) significantly reduced GFAP (A) and Iba1 (B) labeling to levels comparable with those in the sham-vehicle (SV) animals. The data represent the mean ± standard error of the mean (SEM): * P ≤ 0.05, **P ≤ 0.005; scale bar = 100 μm.