Fig. 5

GFAP expression following ICH and blockade or stimulation of the EP1 receptor. Antagonist (SC-51089, 10 µg/kg), agonist (17-pt-PGE₂, 0.3 mg/kg), or no treatment (saline) was administered subcutaneously at the onset of injury, 6 h post-ICH, and at 12-h intervals thereafter. Seventy-two hours after ICH, brains were harvested and sections processed for GFAP immunohistochemistry to evaluate cortical and striatal astrogliosis. a, b Representative high magnification photomicrographs showing the ipsilateral and contralateral a cortex and b striatum for GFAP immunohistochemistry of coronal brain sections from control (left panels), SC-51089- (middle panels), and 17-pt-PGE₂- (right panels) treated mice. Square selections in the insets denote magnified regions. Scale bars on the magnified images and inserts are 100 µm and 2 mm, respectively. c, d Quantification of GFAP immunoreactivity demonstrated that 17-pt-PGE₂-treated mice had significantly less c cortical and d striatal astrogliosis, whereas no significant differences were seen for SC-51089-treated mice. All treatment groups demonstrated negligible staining in the contralateral cortex and striatum; thus, data is presented as the ipsilateral GFAP immunoreactivity corrected for the area of quantification, without normalization for the contralateral equivalent areas. **p < 0.01 and ***p < 0.001 when compared to the control group, n = 8–10 per group.