Objective: To investigate the neuroprotective effect of α2 adrenergic agonist, dexmedetomidine on tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) in brain tissue and serum S-100β protein level in traumatic brain injury rats.
Methods: Seventy-two male Sprague-Dawley rats were randomly divided into sham operation group (group S), traumatic brain injury group (group C), and dexmedetomidine group (group D), 24 rats in each group; each of which was divided into 6, 12, 24 and 48 hours subgroup, 6 rats in each subgroup. Parietal brain contusion was produced by reformed Feeney method. The group S underwent sham operation without blunt force stroke; group D underwent blunt force stroke, then received loading dose of dexmedetomidine, 3 μg/kg with common jugular vein injection and continued infusion with 3 μg·kg(-1)·h(-1) for 2 hours. The total dosage of dexmedetomidine was 9 μg/kg with a volume of 4 ml; group C underwent 0.9% NaCl, 4 ml injection at the same time point with the same method. The S-100 protein activity in arteria cruralis serum was detected at the each time point by ELISA and TNF-α, IL-6 in the brain tissue were detected by ELISA.
Results: There were no significant difference of TNF-α activity among time point of 6, 12, 24 and 48 h in group S ((2.07±0.06), (2.01±0.03), (2.11±0.05), and (2.08±0.04) pg/mg, F=1.147, P>0.05), no significant difference of IL-6 activity among the same time point ((4.03±0.06), (4.07±0.09), (4.06±0.04), and (4.55±0.09) pg/mg, F=1.176, P>0.05), and no significant difference of serum S-100β activity among the same time too ((0.37±0.07), (0.36±0.02), (0.35±0.06), and (0.39±0.11) μg/L, F=1.045, P>0.05). The above indexes in group C were higher than those in group S, and the above indexes in group D were higher than those in group S and lower than those in group C (all P<0.05).
Conclusion: Alpha-2 adrenergic agonist, dexmedetomidine could dramatically inhibit inflammatory reaction induced by traumatic brain injury in rats and protect brain tissue.