Over-expression of PGC-1α reverses mitochondrial function reduction and apoptosis in OGD/R-induced neurons
10.3969/j.issn.1000-4718.2017.11.025
- VernacularTitle:PGC-1α过表达逆转OGD/R诱导的神经元线粒体功能降低和凋亡
- Author:
xia Hui GENG
1
;
ge Ying LI
;
yu Zhen SHI
;
qiang Yong LI
;
Lai WANG
Author Information
1. 河南大学
- Keywords:
Over-expression;
Cortical neurons;
Oxygen-glucose deprivation/reoxygenation;
Apoptosis;
Perox-isome proliferator-activated receptor γ coactivator-1α
- From:
Chinese Journal of Pathophysiology
2017;33(11):2078-2083
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of over-expression of peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α) on mitochondrial morphology and cell apoptosis in the cortical neurons with oxygen glucose depriva-tion/reoxygenation(OGD/R). METHODS:The whole gene sequence of PGC-1α was obtained from the cerebral cortex of C57BL/6 mice by RT-PCR and cloned into the eukaryotic expression vector pEGFP-N1. The pEGFP-N1-PGC-1α was iden-tified by PCR,and transfected into cortical neurons. The level of PGC-1α expression was identified by Western blot. The cortical neurons transfected with pEGFP-N1 and pEGFP-N1-PGC-1α vectors were treated with OGD/R. The mitochondrial mass,reactive oxygen species (ROS) and ATP production,cell apoptosis and changes of cleaved caspase-3 were detected by MitoTracker Red staining,flow cytometry,ATP metabolic assay kit and TUNEL. RESULTS:Over-expression of PGC-1α inhibited the decrease in mitochondrial biogenesis capacity and the ROS formation of OGD/R neurons(P<0.05),en-hanced the ability of ATP synthesis (P<0.01),inhibited neuronal apoptosis (P<0.01) and decreased the activation of caspase-3 (P<0.01). CONCLUSION:PGC-1α over-expression inhibits neuronal apoptosis with OGD/R treatment by promoting mitochondrial biogenesis,inhibiting the production of ROS and maintaining mitochondrial function. PGC-1α may be used as a target for the development of cerebral ischemia/reperfusion injury drugs.
