Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
Figure 7
In situ detection of ROS as using Het. (a) No (Et) signals (red) were detected in control animals. In mice subjected to TBI, a low level of was observed immediately after CCI. By 3 hours this level had increased markedly, remaining high 6 and 24 hours after CCI. (b) Multiple immunofluorescence staining of and cell markers. (Et) signals (red) strongly colocalized with the neuronal marker NeuN (green, upper panel) and to lesser extent with the astroglial marker GFAP (green, lower panel), with nuclei labelled by DAPI (blue). (c) The effect of edaravone treatment on production after CCI ( in each group) is shown. As a control, vehicle was administered 3 hours post-CCI (vehicle 3 h). Edaravone was administered at 0 hours (edaravone 0 h) or 3 hours (edaravone 3 h) after CCI. The production of was evaluated based on the in situ detection of the Et signal (red) in the core-injury area 4 hours after CCI. Nuclei (blue) were labeled with DAPI.
