Selective Inhibition of Janus Kinase 3 Has No Impact on Infarct Size or Neurobehavioral Outcomes in Permanent Ischemic Stroke in Mice

摘要: Janus kinase 3 (JAK3) is associated with the common gamma chain of several interleukin receptors essential to inflammatory signaling. To study potential role JAK3 in stroke-induced neuroinflammation, we subjected mice permanent middle cerebral artery occlusion, and investigated effects inhibition decernotinib (VX-509) on infarct size, behavior, levels mediators. Results from our double immunofluorescence staining showed expression neurons, endothelial cells, microglia/macrophages ischemic mouse brain (n=3). We found for first time that total as well phosphorylated/activated are dramatically increased after stroke ipsilateral hemisphere (**P<0.01; n=5-13/group) addition IL-21 n=5-7/group). However, confirmed by reduced phosphorylation its activation loop at tyrosine residues 980/981 does not reduce volume measured 48 h (n=6-10/group) nor it alter behavioral outcomes sensitive neurological deficits or neuroinflammatory response (n=9-10/group). These results do support a detrimental acute neuroinflammation following focal ischemia. The functional remains be further investigated.