Sevoflurane preconditioning protects against spinal cord ischemia/reperfusion injury by up-regulating miR-199a-5p in rats
10.3969/j.issn.1001-1978.2018.09.010
- VernacularTitle:七氟烷预处理上调miR-199a-5p对脊髓缺血/再灌注损伤的保护作用
- Author:
Ning BAO
1
;
Hong MA
Author Information
1. 中国医科大学附属第一医院麻醉科
- Keywords:
sevoflurane preconditioning;
ischemia-reperfusion injury;
spinal cord;
miR-199a-5p;
apopto-sis;
blood-spinal cord barrier
- From:
Chinese Pharmacological Bulletin
2018;34(9):1230-1234
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of sevoflurane preconditioning on spinal cord ischemia-reperfusion in-jury ( SCIRI ) of miR-199a-5p in rats. Methods Twenty-four SD rats were randomly divided into: group of sham ( Sham group) , group of ischemia-reperfusion ( I/R group ) , and group of sevoflurane and control ( SEVO+I/R group) . Sham group received the same operation, but did not inhale sevoflurane or close the aortic arch; SCIRI model was established after 14 min of the aortic arch of the non-invasive arterial clip in I/R group. SEVO+I/R group, before the establishment of SCIRI model, was inhaled 2.4% sevoflurane for 3 h. Basso Beattie Bresnahan scoring method was used to evaluate neuromotor function and TUNEL staining to observe apoptosis. Evans blue ( EB) was used to de-termine blood-spinal cord barrier ( BSCB) permeabili-ty; real-time qPCR to detect miR-199a-5p content;Western blot to measure the levels of caspase-9 and Bcl-2 in spinal cord tissues. Results Compared with sham group, the score of neuromotor function in I/R group decreased, cell apoptosis rate increased, BSCB permeability increased, miR-199a-5p expression de-creased, caspase-9 expression increased, and Bcl-2 expression decreased; compared with I/R group, the neurological motor function score of SEVO+I/R group increased, the apoptotic rate decreased, the BSCB per-meability decreased, the expression of miR-199a-5p increased, the expression of caspase-9 decreased, and the expression of Bcl-2 increased. Conclusion Sevoflurane pretreatment may reduce BSCB permeabili-ty and neuronal apoptosis by up-regulation of miR-199a-5p and protection of SCIRI in rats.
