Fig. 2

dBET1 ameliorates ischemia-induced neurological deficits. A Schematic illustration of the experimental design. Adult male C57BL/6 mice were injected intraperitoneally with dBET1 (30 mg/kg) at 4 and 24 h after 35-min transient middle cerebral artery occlusion (tMCAO); the body weight and neurobehavioral tests were examined at indicated timepoints. B Neurological deficit score was assessed using six individual functional tests, where a lower value indicates a better function. The dBET1 treated ischemic mice exhibited a dramatically reduced neurological deficit score compared to controls in overall or individual scores. Veh: n = 14; dBET1: n = 12. C No significant baseline difference was detected between groups in the vertical grid test. The dBET1 treated mice used much less time (about 54% reduction) to climb down from the top of the apparatus than vehicle controls, which is closer to baseline level. Veh: n = 14; dBET1: n = 12. D No significant baseline difference was found between groups in the total traveled distance in the open field test. After stroke, the mice traveled much less distance, which is more evident in the dBET1 treated group. Representative tracking maps and corresponding heat maps indicate the time of animal spent per location in the open field paradigm. Veh: n = 14; dBET1: n = 12. E dBET1 significantly decreased the loss of body weight over 48 h after tMCAO. Veh: n = 14; dBET1: n = 12. *P < 0.05, **P < 0.01, ***P < 0.001. Veh, vehicle