Protective effect and mechanism of hydrochloride dexmedetomidine on the severe craniocerebral trauma in rats

To investigate the cerebral protection effect of dexmedetomidine (DEX) in severe craniocerebral injury rat model. A total of 120 male SD rats were equally randomly divided into DEX group, sham group, and control. Rat acute severe craniocerebral injury model was established using hydraulic blow method. The rats received sedative treatment at 2 h after injury. Rat behavior changes before and after modeling were observed. Serum S-100β, neuron specific enolase (NSE), and myelin basic protein (MBP) levels on pre-operation (T1), day 1 post operation (POD1, T2), day 3 post operation (POD3, T3), day 5 post operation (T4), and day 7 post operation (T5) were detected by ELISA. Rat hippocampus was extracted for pathological section on T2, T3, T4, and T5. Neuronal cell death was observed upon Nissl’s staining. NF-κB and Caspase-3 expression in hippocampus were tested by immunohistochemistry. Serum S-100β, NSE, and MBP levels significantly decreased on T2, T3, T4, and T5 in DEX group compared with control group (P < 0.05). Neuronal cell death, NF-κB, and Caspase-3 expression markedly reduced on T2, T3 (except NF-κB), T4, and T5 in DEX group compared with control group (P < 0.05). DEX can protect brain upon improving cerebral oxygen metabolism and alleviating cerebral ischemia hypoxia in severe craniocerebral injury.