Effect of sevoflurane preconditioning on autophagy after traumatic brain injury in rats: the role of JNK signaling pathway
10.3760/cma.j.issn.0254-1416.2014.08.028
- VernacularTitle:七氟醚预处理对大鼠创伤性脑损伤后自噬的影响:JNK信号通路在其中的作用
- Author:
Lirong HUANG
;
Xiangrong CHEN
;
Hefan HE
;
Zhiyuan CHEN
;
Jinwei LIANG
- Publication Type:Journal Article
- Keywords:
Anesthetics,inhalation;
Craniocerebral trauma;
Autophagy;
Mitogen-activated protein kinases
- From:
Chinese Journal of Anesthesiology
2014;34(8):1007-1011
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of sevoflurane preconditioning on autophagy after traumatic brain injury (TBI) in rats and the role of C-Jun N-terminal kinase (JNK) signaling pathway.Methods Sixty adult male Sprague-Dawley rats,weighing 220-250 g,were randomly divided into 4 groups (n =15 each) using a random number table:sham operation group (group S),group TBI,TBI + sevoflurane preconditioning group (group TBI + Sevo) and TBI + sevoflurane preconditioning + JNK inhibitor SP600125 group (group TBI + Sev + SP).TBI models were established using Feeney' s method.In TBI + Sev and TBI + Sev + SP groups,the rats inhaled 2.4％ sevoflurane for 30 min once a day for 4 concecutive days,and TBI was produced at 24 h after the end of sevoflurane preconditioning.In TBI + Sev + SP group,SP600125 (6 mg/kg) was injected intrapetitoneally at 30 min after TBI.Five rats were chosen at day 1,3,and 7 after TBI,and neurological deficit score (NDS) was measured.The rats were then sacrificed and brains were removed to measure brain water content,expression of LC3 lⅡ and Beclin-1 mRNA (using PCR),and expression of LC3 Ⅱ,Beclin-1,JNK and phosphorylated JNK (p-JNK) (by Western blot).Results Compared with group S,brain water content and NDS were significantly increased,and the expression of LC3 Ⅱ and Beclin-1 protein and mRNA,JNK,and p-JNK was up-regulated in the other three groups.Brain water content and NDS were significantly decreased,and the expression of LC3 Ⅱ and Beclin-1 protein and mRNA,JNK,and p-JNK was down-regulated in TBI + Sev and TBI + Sev + SP groups as compared with group TBI,and in TBI + Sev + SP group as compared with TBI + Sev group.Conclusion The mechanism by which sevoflurane preconditioning mitigates TBI is related to inhibiton of activation of JNK signaling pathway and decreased autophagy in rats.
