Abstract
Traumatic brain injury (TBI) affects 1.9 million Americans, including blast TBI that is the signature injury of the Iraq and Afghanistan wars. Our project investigated whether stromal vascular fraction (SVF) can assist in post-TBI recovery. We utilized strong acoustic waves (5.0 bar) to induce TBI in the cortex of adult Rowett Nude (RNU) rats. One hour post-TBI, harvested human SVF (500,000 cells suspended in 0.5 mL lactated Ringers) was incubated with Q-Tracker cell label and administered into tail veins of RNU rats. For comparison, we utilized rats that received SVF 72 h post-TBI, and a control group that received lactated Ringers solution. Rotarod and water maze assays were used to monitor motor coordination and spatial memories. Rats treated immediately after TBI showed no signs of motor skills and memory regression. SVF treatment 72 h post-TBI enabled the rats maintain their motor skills, while controls treated with lactated Ringers were 25% worse statistically in both assays. Histological analysis showed the presence of Q-dot labeled human cells near the infarct in both SVF treatment groups; however, labeled cells were twice as numerous in the one hour group. Our study suggests that immediate treatment with SVF would serve as potential therapeutic agents in TBI.
Highlights
Traumatic brain injury (TBI) is a severe injury that affects up to 3.8 million Americans each year with many more TBI incidents going unreported [1]
The stromal vascular fraction (SVF) used in this project was analyzed by flow cytometry to determine the amount of adipose
The SVF used in this project was analyzed by flow cytometry to determine the amount of adipose derived stem cells (ADSC) and hematopoietic stem cells (HSC) found within our sample
Summary
Traumatic brain injury (TBI) is a severe injury that affects up to 3.8 million Americans each year with many more TBI incidents going unreported [1]. Blast waves, resulting from overpressures created by explosive devices, can cause a TBI due to rapid and extreme changes in atmospheric pressure. These changes can cause tissues, like those in the brain, to be displaced, stretched and sheered, resulting in a blast TBI [4]. This disruption in the cerebral vasculature prevents adequate blood flow to neuronal cells, which can eventually become depleted of oxygen, nutrients and eventually die via necrosis and apoptosis [5,6]. Neuronal injury and death are directly associated with the short-term symptomatic effects (dizziness, severe headaches and complete loss of consciousness) and the long-term effects (memory loss, depression and suicidality) [7]
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