Fig. 1

IL-1α conveys direct neuroprotection both in vitro (a, b) and in vivo (c–h) when delivered acutely. Primary cortical neurons under two forms of cytotoxic stress: a OGD or b 20 μM NMDA. Excess IL-1α concentrations are cytotoxic while moderate doses conveyed direct protection from oxygen-glucose deprivation (OGD) as well as NMDA-based toxicity (n = 9 per group). Mice treated with IA IL-1α have c fewer apoptotic cells in the infarct and peri-infarct regions than vehicle and IV IL-1α treated mice 3 days following stroke. d Quantification of TUNEL and e cresyl violet stains (representative images of stained sections depicted above each bar). Mice treated with IA IL-1α have reduced infarct volumes on PSD 3 compared to control mice. c Scale = 200 μm (n = 3 per group). Mice treated with IA IL-1α less microglial activation in the peri-infarct regions than vehicle or IV IL-1α treated mice on PSD 7 (f, g). Representative images of CD11b (green) staining showing less overall microglial staining in the peri-infarct region of treated animals on PSD 7 compared to controls; inset showing magnified representing images (f) (n = 4 per group). Scale = 50 μm. Quantification of CD11b stains (g). IL-1α enhances functional recovery following stroke. Mice were evaluated for functional performance by using total distance traveled in an open field free movement paradigm (h). Mice were evaluated for a baseline measurement the day prior to stroke surgery and then evaluated for functional recovery on PSD 1 and PSD 7. Mice treated with IA or IV IL-1α show better functional outcome than control mice (n = 5 per group). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Data are the mean ± SEM