Neuroprotective effects and mechanism of ethanol extract of Cistanche tubulosa against oxygen-glucose deprivation/reperfusion.
10.19540/j.cnki.cjcmm.20181214.001
- Author:
Jing-Kang WANG
1
;
Li-Chao WANG
1
;
Yong JIANG
1
;
Peng-Fei TU
1
;
Ke-Wu ZENG
1
Author Information
1. State Key Laboratory of Natural and Biomimetic Drugs,Peking University Beijing 100191,China.
- Publication Type:Journal Article
- Keywords:
Cistanche tubulosa;
ethanol extract;
mitochondri al pathway;
neuronal injury;
oxygen-glucose deprivation/reperfusion(OGD/R)
- MeSH:
Animals;
Apoptosis;
Caspase 3;
metabolism;
Cistanche;
chemistry;
Ethanol;
Glucose;
Neuroprotective Agents;
pharmacology;
Oxidative Stress;
Oxygen;
PC12 Cells;
Plant Extracts;
pharmacology;
Poly (ADP-Ribose) Polymerase-1;
metabolism;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Rats;
bcl-2-Associated X Protein;
metabolism
- From:
China Journal of Chinese Materia Medica
2019;44(13):2686-2690
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the inhibitory effects and mechanism of Cistanche tubulosa ethanol extract( CTEE) against oxygen-glucose deprivation/reperfusion( OGD/R)-induced PC12 cells neuronal injury. In this study,OGD/R-induced PC12 cells were used to explore the neuroprotective effects of CTEE( 12. 5,25,50 mg·L-1) by detecting cell viability with MTT assay,apoptosis with AO/EB and Hoechst 33258,mitochondrial membrane potential changes with JC-1 staining,mitochondrial oxidative stress with MitoSOX staining,as well as the apoptosis-related protein expression( PARP,cleaved PARP,caspase-3,cleaved caspase-3,Bax,Bcl-2) with Western blot. RESULTS:: showed that CTEE effectively protected OGD/R-induced neuronal injury and increased the survival rate of PC12 cells.AO/EB and Hoechst 33258 staining showed that CTEE could effectively inhibit apoptosis. Moreover,JC-1 and MitoSOX staining results showed that CTEE decreased mitochondrial stress and mitochondrial membrane potential imbalance in PC12 cells in a concentration-dependent manner. Meanwhile,CTEE could obviously suppress the activation of key proteins in mitochondrial apoptosis pathway such as caspase-3 and PARP,and significantly inhibit the rise of Bax and down-regulation of Bcl-2. In conclusion,CTEE has obvious protective effects on OGD/R-induced PC12 cells neuronal injury,potentially via inhibiting mitochondrial oxidative stress and apoptosis-related signaling pathway.
