Brain Cooling-Stimulated Angiogenesis and Neurogenesis Attenuated Traumatic Brain Injury in Rats

BACKGROUND: Although brain cooling has been reported to be effective in improving the outcome after traumatic brain injury (TBI) in rats, the mechanisms of brain cooling-induced neuroprotective actions remain unclear. This study was to test whether angiogenesis and neurogenesis attenuating TBI could be brain cooling stimulated. METHODS: Anesthetized rats, immediately after the onset of TBI, were divided into two groups and given the brain cooling (infusing 5 mL of 4°C saline via the external jugular vein) or no brain cooling (infusing 5 mL of 37°C saline via the external jugular vein). RESULTS: Brain cooling without interference with the core temperature in rats significantly attenuated TBI-induced cerebral infarction (90 mm³ vs. 250 mm³) and motor (61 degrees vs. 57 degrees maximal angle) and proprioceptive (14% vs. 42% maximal possible effect) function deficits, significantly reduced TBI-induced neuronal (24 vs. 62 neuronal-specific nuclear [NeuN]-TUNEL double-positive cells) and glial (5 vs. 35 GFAP-TUNEL double-positive cells) apoptosis (increased TUNEL-positive and caspase-3-positive cells), neuronal loss (102 vs. 66 NeuN-positive cells), and gliosis (40 vs. 66 GFAP-positive cells; 66 vs. 89 Iba1-positive cells), and significantly promoted angiogenesis (5-bromodeoxyuridine [BrdU]/endothelial cells vs. 1-BrdU/endothelial cell; 58 vs. 31 vascular endothelial growth factor-positive cells), and neurogenesis (33 vs. 14 BrdU/NeuN positive cells). CONCLUSIONS: Brain cooling-stimulated angiogenesis and neurogenesis attenuated a fluid percussion TBI in rats.