Traumatic brain injury (TBI) is a common cause of morbidity and mortality in the civilian population. The purpose of this study is to examine the effect(s) of ASC treatment on cellular and functional recovery in TBI via both in vitro and in vivo methods.
Cultured neuroblastoma cells, SH-SY5Y, were scratched to mimic TBI in an in vitro model. The effect of ASC conditioned medium on cell death, mitochondrial function, and expression of inflammatory cytokines (TNF-α, IL-1β and IL-6) as well as apoptosis marker FAS was measured. In our in vivo model, Sprague-Dawley rats underwent TBI via a frontal, closed head injury model. Animals randomly received either intravenous human derived ASCs or intravenous saline within 3 hours of injury, and were compared to a Sham group. Functional recovery was evaluated via accelerating Rotarod method. On post-TBI day 3, brain tissue was harvested and assessed for cellular damage via ELISA assay for TNF-α, as well as immunohistochemical staining for β-APP.
Our in vitro data show that ASC treatment imparted reduced cell death (Ratio to control: 1.21±0.066 vs. 1.01±0.056, p=0.017), increased cell viability (Ratio to control: 0.86±0.009 vs. 1.09±0.01, p = 0.0001), increased mitochondrial function (Percentage of Control: 78±6% vs. 68±3%), and significantly decreased levels of inflammatory cytokine IL-1β. In our in vivo study, compared to TBI alone, ASC treated animals showed no difference in functional recovery, lower levels of expressed TNF-α (Ratio to total protein: 0.47±0.01 vs. 0.67±0.04; p<0.01) and lower levels of β-APP (Flourescence ratio: 0.43±0.05 vs. 0.69±0.03; p<0.01).
ASC treatment results in improved cell survival, decreased inflammatory marker release, and decreased evidence of neural injury. No difference in functional recovery was seen. These data suggest the potential for ASC treatment to aid in cellular protection and recovery in neural cells following TBI.
Level IIStudy Type: Therapeutic/Care Management.
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