Rg1 alleviates the damage in ALS model through regulation of miR153/Nrf2/HO-1
10.16438/j.0513-4870.2017-1012
- VernacularTitle:人参皂苷Rg1调控miR-153/Nrf2/HO-1减轻肌萎缩侧索硬化模型小鼠损伤
- Author:
Zhao ZHANG
1
;
Sha-sha WANG
1
;
Tian-bi ZHU
1
;
Shi-feng CHU
1
;
Nai-hong CHEN
1
Author Information
1. State Key Laboratory of Bioactive Substances and Functions of Natural Medicine, Neuroscience Center, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing 100050, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
amyotrophic lateral sclerosis;
ginsenoside Rg1;
oxidative stress damage;
NF-E2-related factor 2;
miR-153
- From:
Acta Pharmaceutica Sinica
2018;53(4):546-552
- CountryChina
- Language:Chinese
-
Abstract:
The impact of Rg1 in the disease progress and pathology of amyotrophic lateral sclerosis (ALS) was investigated in mouse model (SOD1 G93A). Body weight and survival rate were monitored to check the course of disease. Rotarod test was used to evaluate the coordination of muscle movement. Toluidine blue staining and immunofluorescence were used to check the effect of Rg1 on motor neuron and microglia. The expression of oxidative stress related protein Nrf2 and the miRNA were tested to investigate the mechanism of Rg1. We found that 20 mg·kg-1·d-1 Rg1 significantly postponed the disease onset and process, improved the motor syndrome, reduced the loss of motor neuron and inhibited the activation of microglia cells. Rg1 inhibited the aggregation of miR-153 in the spinal cord of ALS mice, which relieved the inhibition of Nrf2 and contributed to its up-regulation in the activation of HO-1 anti-oxidative signal pathway. Our study confirmed that Rg1 could protect ALS mice from oxidative damage through the up-regulation of miR-153/Nrf2/HO-1, which provides a theoretical foundation for Rg1 application to the ALS treatment.
