Figure 1
Effect of AT2 activation with C21 on blood pressure, neurological outcome, lesion volume and cerebral inflammation: Vehicle-treated WT mice (n = 9; white) were compared to WT mice treated with low (0.03 mg/kg; LD C21; n = 9; red), or high dose (0.1 mg/kg; HD C21; n = 9; black) of C21; the data are expressed as mean ± SD; n.s. = not significant. (A) Peritraumatic systolic blood pressure (time point 0 during anesthesia, postoperative in awake animals): while there were no significant changes of blood pressure in the vehicle and LD groups, in the HD group there was a limited drop of blood pressure 2 h after CCI compared to the vehicle-treated group (*p = 0.035). At later time points, the values were within physiological levels, independent of the treatment. (B) NSS: one day (24 h) after TBI in all treatment groups, there was a significant increase in the neurological impairment followed by a significant improvement the following days in all groups. Treatment with C21 in both dosages did not affect neurologic outcome compared to the vehicle. (C) The cerebral lesion volume 5 days after TBI (5 days post-injury, dpi; to rule out effects of edema, data are expressed as % contralateral hemisphere) was elevated compared to the primary lesion (p < 0.05; see results section); however, there was no difference between treatment groups. (D) Five days after TBI (5 dpi), the perilesional gene expression of the cytokine IL1β was not affected by AT2 activation with C21 in both dosages compared to the vehicle treatment.
