Brain cooling-stimulated angiogenesis and neurogenesis attenuated traumatic brain injury in rats

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.

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).

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).

Brain cooling-stimulated angiogenesis and neurogenesis attenuated a fluid percussion TBI in rats.