註釋 Introduction:The inflammatory reaction following cerebral ischemia comes along with immigration and activation of immune cells which has substantial impact on the final brain damage. In our study, we show that the transcription factor NR4A1 has a crucial influence within strokes pathophysiology as mice devoid of NR4A1 show worsened functional outcome and increased infarct volumes when compared to wildtype mice. As our data suggest an anti-inflammatory role for NR4A1, we hypothesised that NR4A1-activation by its agonist Cytosporone-B limits ischemia-induced immune response and infarct expansion. Methods:Wildtype (n=43) and NR4A1-deficient (n=8) mice were subjected to occlusion of the MCA (MCAO, 30 min). Animals were injected with Cytosporone-B (13 mg/kg, i.p.) 3h (n=21) or 12h (n=14) after reperfusion. Mice were tested for functional outcome and infarct volume, gene-expression and neutrophil immigration were analyzed via RT-PCR, histology and FACS.Results:Mice devoid of NR4A1 showed worsened functional outcome (p 