Topical application of the hematostatic agent Surgiflo® could attenuate brain injury in experimental TBI mice

The pathologies resulting from traumatic brain injury (TBI) have been thoroughly studied, but rarely have the effects of bleeding and coagulation in the early stage of TBI been considered. In this study, we investigated the effects of topical Surgiflo^® application on brain injury in experimental TBI mice using S100β, MAP-2 and mNSS scores.

TBI was induced by modified weight drop injury in male C57BL/6 mice. The mice were then randomly divided into (i) the sham group, (ii) TBI mice applied with saline (vehicle), and (iii) TBI mice applied with Surgiflo^® in the same volume. Modified neurological severity scores (mNSS) were measured on days 0 (before surgery), 1, 3, 7, and 28 to evaluate neurologic functional deficits. At day 28, the mice were sacrificed, and the forebrains were sliced. The effects of Surgiflo^® on microtubule-associated protein 2 and serum S100β protein were examined by immunohistochemistry and electro-chemiluminescence immunoassay.

Serum S100β protein levels were significantly elevated at different time points (24 h, 3 days, 7 days) in the TBI groups (p  <  0.01) compared to normal control groups. Surgiflo^® induced a lower concentration of serum S100β protein levels at day 3 (p < 0.05) and day 7 (p < 0.05) compared to the TBI group applied with saline. H&E staining showed that Surgiflo^® treatment led to a 45% decrease in cortical brain lesion volume and in subcortical white matter 28 days after TBI. Compared with the saline-treated group, the number of MAP2-positive cells was significantly increased in the perilesional area of the Surgiflo^®-treated group. The Surgiflo^®-treated group exhibited lower mNSS scores on days 7 and 28 than did the saline-treated group.

Surgiflo^® treatment produced a significant decrease in serum S100β protein levels in TBI mouse models, which may lead to an improvement in the recovery of TBI models.