Fig. 1

Neurological deficits after TBI. Neurological effects of TBI were assessed by a mNSS, b Rotarod, and c open-field behavioral task tests prior to and 12, 24, and 48 h post-TBI. a mNSS scores were significantly higher in the TBI groups relative to those in the sham groups. The mNSS scores were maximal at 24 h and gradually decreased with time in the TBI group. No significant difference was observed between the caspase-1^−/− and WT-TBI group at 12 h. However, the caspase-1^−/− group showed significantly lower mNSS scores relative to the WT-TBI group at 24 and 48 h post-TBI. b Rotarod scores were minimal at 24 h and gradually increased with time in WT-TBI group. Relative to WT-TBI mice, TBI-induced impaired Rotarod performance was attenuated in the caspase-1^−/− mice at 24 and 48 h after TBI. c In the open-field task, all mice traveled the same distance in the center zone compared to the perimeter zone. WT-TBI mice spent less time in the perimeter zone of the open-field chamber compared to caspase-1^−/−-TBI mice. Total travel distance was significantly different between WT-TBI and caspase-1^−/−-TBI mice. d TUNEL staining was used to detect cortical damage in our TBI model. Apoptosis index, the number of TUNEL-positive cells divided by the total cells per field, was examined. Each AI was assessed in 20 randomly selected fields. Data are presented as the mean ± SEM. **p < 0.01 and ***p < 0.001 versus sham group, #p < 0.05 and ##p < 0.01, compare to TBI group (n = 11) (mNSS, Rotarod, and open-field)