Abstract

Objective To evaluate the effect of dexmedetomidine on autophagy in the hippocampal neurons of rats with traumatic brain injury (TBI). Methods Adult male Sprague-Dawley rats, aged 12-16 weeks, weighing 340-370 g, were randomly divided into 3 groups (n= 80 each) using a random number table: sham operation group (group S), traumatic brain injury group (group TBI) and dexmedetomidine group (group Dex). The rats were subjected to a diffuse cortical impact injury caused by a modified weight-drop device to induce TBI.Dexmedetomidine 15 μg/kg was injected intravenously immediately after TBI in Dex group.At 24 and 48 h after TBI, neurological deficit score (NDS) was assessed, Morris water maze test was performed, and brains were removed for detection of brain water content in the brain tissue.At 6, 12, 24 and 48 h after TBI, the expression of hippocampal LC3Ⅱ was determined using Western blot analysis. Results Compared with group S, brain water content and NDS were significantly increased at 24 and 48 h after TBI, the escape latency was prolonged, and the expression of hippocampal LC3Ⅱ was up-regulated at 6, 12, 24 and 48 h after TBI in TBI group.Compared with TBI group, brain water content and NDS were significantly decreased at 24 and 48 h after TBI, the escape latency was shortened, and the expression of hippocampal LC3Ⅱ was down-regulated at 6, 12, 24 and 48 h after TBI in Dex group. Conclusion The mechanism by which dexmedetomidine reduces TBI is related to inhibition of autophagy in the hippocampal neurons of rats. Key words: Dexmedetomidine; Brain injury; Autophagy; Hippocampus; Neurons

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