Tetrahydroxystilbene glucoside protects against sodium azide-induced mitochondrial dysfunction in human neuroblastoma cells
10.1016/j.chmed.2020.11.007
- Author:
Ru-yi ZHANG
1
;
Lan ZHANG
1
;
Lin LI
1
;
Xu ZHANG
2
;
Yan-chuan WU
2
;
Xue-jing SUN
3
Author Information
1. Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing Engineering Research Centre for Nerve System Drugs, Beijing Institute for Brain Disorders, Key Laboratory for Neurodegenerative Diseases of Ministry of Education
2. Department of Central Laboratory, Xuanwu Hospital of Capital Medical University
3. Department of Haematology, Xuanwu Hospital of Capital Medical University
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
mitochondria;
sodium azide;
tetrahydroxystilbene glucoside
- From:
Chinese Herbal Medicines
2021;13(2):255-260
- CountryChina
- Language:Chinese
-
Abstract:
Objective: Mitochondrial dysfunction is evident in the early stage of Alzheimer's disease (AD). Therefore development of drugs that protect mitochondrial function is a promising strategy for AD. The present work was to investigate the effects of 2, 3, 5, 4′-Tetrahydroxystilbene-2-O-β-d-glucosides (TSG) on a mitochondrial dysfunction cell model induced by sodium azide and elucidate the underlying mechanisms. Methods: Mitochondrial membrane potential (MMP) was detected by a fluorescence method. Cellular adenosine triphosphate (ATP) level was measured using a firefly luciferase-based kit. Reactive oxygen species (ROS) was detected using dichlorofluorescin diacetate (DCFH-DA). The expression levels of Bcl-2 and Bax were measured by Western blotting assay. Flow cytometry was utilized to measure apoptosis. Results: Pretreatment of TSG (25–200 μmol/L) for 24 h significantly elevated MMP and ATP content, reduced ROS level and Bax/Bcl-2 ratio, and inhibited apoptosis in SH-SY5Y cells exposed to sodium azide. Conclusion: These results suggest that TSG protects SH-SY5Y cells against sodium azide-induced mitochondrial dysfunction and apoptosis. These findings are helpful to understand the protective effect of TSG on mitochondria, which are involved in the early stage of AD.
