Fig. 3
TMF-treated and AHRcKO mice showed downregulated microglia and astroglial activation at 48 h after MCAO. a Representative immunohistochemical staining for neuroinflammation at the peri-infarct cortex (bregma = + 0.86 mm) of normal WT (n = 6/each group), poststroke WT-Vehicle treated, WT-TMF treated, normal AHRcKO, poststroke AHRflx/flx, and AHRcKO mice. The inset in low magnification is shown with a high magnification view in the next row(s). At high magnification, note the increase in AHR immunoreactivity colocalized within Iba1-positive microglia and GFAP-positive astrocytes (red arrows) in the WT-Vehicle-treated and AHRflx/flx mice after MCAO, which was markedly decreased in the WT-TMF-treated and AHRcKO mice (whose AHR spared in microglia), respectively. Furthermore, increased Iba1-positive microgliosis and GFAP-positive astrogliosis in the WT-Vehicle and AHRflx/flx mice after MCAO were significantly decreased in the WT-TMF-treated and AHRcKO mice (whose AHR deleted in astroglia), respectively. Intracellular AHR immunoreactivity was predominantly in the nucleus, and to a lesser extent in the cytoplasm. Quantification of the relative immunereactive are stained with AHR (b), Iba-1(c), and GFAP (d). #p < 0.05 compared with the respective normal controls.*p < 0.05 WT-TMF compared with WT-Vehicle; AHRcKO compared with AHRflx/flx. The scale bars represent 60 μm at low magnification and 8 μm at high magnification