Fig. 3.
The thalidomide analog 3,6′-DT treatment decreases glial activation, cell adhesion molecule expression, and neutrophil infiltration after ischemic stroke. A: Examples of immunoreactivity for markers of activated microglia (Iba-1), astrocytes (GFAP), neutrophils (MPO), and the vascular endothelial cell adhesion molecule ICAM-1 in the cerebral cortex of mice from the indicated treatment groups. B–D: Results of quantification of numbers of cells immunoreactive with Iba-1 (B), GFAP (C), and MPO (D) in the ipsilateral cerebral cortex at 72 hr poststroke. E: Immunoblot showing examples of relative levels of ICAM-1 in tissue samples from cortex in vehicle-treated or 3,6′-DT-treated mice at 72 hr after ischemic stroke. F: Results of densitometry analysis of ICAM-1 immunoblots (n = 6 mice per group). The mice were treated with either vehicle or 56 mg/kg 3,6′-DT 1 hr prior to MCAO/R. *P < 0.05, **P < 0.01, ***P < 0.001 compared with the value for sham mice. #P < 0.05, ##P < 0.01 compared with the value for vehicle-treated mice. Scale bar = 50 μm. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]