Remote ischemic preconditioning promotes mitochondrial biosynthesis and protects cerebral ischemia-reperfusion injury in rats via AMPK/PGC-1α signaling pathway
10.3760/cma.j.issn.1673-4165.2022.06.005
- VernacularTitle:远隔缺血预适应通过AMPK/ PGC-1α信号通路促进线粒体生物合成保护脑缺血再灌注损伤大鼠
- Author:
Lei ZHANG
1
;
Weiqiong YUAN
;
Xiangli KONG
;
Junchao LI
;
Bei ZHANG
Author Information
1. 西安医学院第一附属医院神经内科，西安 710000
- Keywords:
Brain ischemia;
Reperfusion injury;
Ischemic preconditioning;
AMP-activated protein kinases;
Peroxisome proliferator-activated receptor γ coactivator 1-α
- From:
International Journal of Cerebrovascular Diseases
2022;30(6):426-432
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective mechanism of remote ischemic preconditioning (RIPC) on cerebral ischemia-reperfusion (I/R) injury in rats.Methods:Forty-eight SD rats were randomly divided into sham operation group, RIPC group, I/R group, RIPC+I/R group, and compound C group ( n=9 in each group). The neurological function score, cerebral infarction volume (TCC staining) and neuronal apoptosis rate (TUNEL staining) were measured. The activity of superoxide dismutase (SOD) 2 and malondialdehyde level in homogenate of brain tissue were detected. Expression levels of AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α signaling pathway-related proteins in brain tissue were detected by Western blot. Results:The neurological deficit score, cerebral infarction volume and neuron apoptosis rate in the I/R group were significantly higher than those in the sham operation group (all P<0.05). Compared with the I/R group, the neurological deficit score, cerebral infarction volume and neuron apoptosis rate in the RIPC+I/R group were significantly decreased (all P<0.05). Compared with the RIPC+I/R group, the neurological deficit score, cerebral infarction volume and neuron apoptosis rate in the compound C group were significantly increased (all P<0.05). Compared with the sham operation group, the SOD activity in the I/R group was significantly decreased, and the malondialdehyde content was significantly increased (all P<0.05). Compared with the I/R group, the SOD activity in the RIPC+I/R group was significantly increased, and the malondialdehyde content was significantly decreased (all P<0.05). Compared with the RIPC+I/R group, the SOD activity in the compound C group was significantly decreased, and the malondialdehyde content was significantly increased (all P<0.05). Compared with the sham operation group, the expressions of AMPK, p-AMPK, PGC-1α, nuclear respiratory factor (NRF)-1, mitochondrial transcription factor A (TFAM), SOD2, uncoupling protein 2 (UCP2), cytochrome C (CytC), and apoptosis-inducing factor (AIF) in the brain tissue of the I/R group were significantly increased (all P<0.05). Compared with the I/R group, the expressions of AMPK, p-AMPK, PGC-1α, NRF-1, TFAM, SOD2 and UCP2 in the ischemic brain tissue of the RIPC+I/R group were significantly increased, while the expressions of CytC and AIF were significantly decreased (all P<0.05). Compared with the RIPC+I/R group, the expressions of AMPK, p-AMPK, PGC-1α, NRF-1, TFAM, SOD2 and UCP2 in the brain tissue of the compound C group were significantly decreased, while the expressions of CytC and AIF were significantly increased (all P<0.05). Conclusions:RIPC has a protective effect on I/R injury. Its mechanism may be associated with the activation of AMPK/PGC-1α signaling pathway and maintaining mitochondrial biogenesis.
