Effect of dexmedetomidine on autophagy in hippocampal neurons of rats with traumatic brain injury
10.3760/cma.j.issn.0254-1416.2015.03.029
- VernacularTitle:右美托咪定对创伤性脑损伤大鼠海马神经元自噬的影响
- Author:
Manhe ZHANG
;
Xiumin ZHOU
;
Yanjie XING
;
Dong CHEN
;
Shidong KANG
;
Jie LIU
- Publication Type:Journal Article
- Keywords:
Dexmedetomidine;
Brain injury;
Autophagy;
Hippocampus;
Neurons
- From:
Chinese Journal of Anesthesiology
2015;35(3):373-376
- CountryChina
- Language:Chinese
-
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 LC3]Ⅱ 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 LC3 Ⅱ was upregulated 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 LC3 Ⅱ 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.
