YGS40, an active fraction of Yi-Gan San, reduces hydrogen peroxide-induced apoptosis in PC12 cells.
10.1016/S1875-5364(15)30037-6
- Author:
Yu-Rong ZHAO
1
;
Wei QU
1
;
Wen-Yuan LIU
2
;
Hao HONG
3
;
Feng FENG
4
;
Han CHEN
5
;
Ning XIE
6
Author Information
1. Department of Natural Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, China.
2. Department of Pharmaceutical Analysis, China Pharmaceutical University, Nanjing 210009, China.
3. Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: honghao@cpu.edu.cn.
4. Department of Natural Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, China. Electronic address: fengsunlight@163.com.
5. New Technology Center of Chemical Pharmaceutical Shanghai Institute of Pharmaceutical Industry China State Institute of Pharmaceutical Industry, Shanghai 200437, China.
6. Jiangxi Qingfeng Pharmaceutical Corporation, Ganzhou 341000, China.
- Publication Type:Journal Article
- Keywords:
Antioxidant effects;
Apoptosis;
Hydrogen peroxide;
YGS40;
Yi-Gan San
- MeSH:
Animals;
Antioxidants;
pharmacology;
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cell Survival;
drug effects;
Drugs, Chinese Herbal;
pharmacology;
Hydrogen Peroxide;
toxicity;
Malondialdehyde;
metabolism;
Mitochondria;
drug effects;
enzymology;
metabolism;
Neuroprotective Agents;
pharmacology;
Oxidative Stress;
drug effects;
PC12 Cells;
Rats;
Reactive Oxygen Species;
metabolism
- From:
Chinese Journal of Natural Medicines (English Ed.)
2015;13(6):438-444
- CountryChina
- Language:English
-
Abstract:
In our previous study, we have elucidated the chemical profile of YGS40, a fraction of Yi-Gan San (YGS), used for the treatment of Alzheimer's disease (AD). Oxidative stress-induced apoptosis is implicated in neurodegenerative disorders such as AD. The aim of the present study was to explore the protective effects of YGS40 against hydrogen peroxide (H2O2)-induced apoptosis in PC12 cells and the underlying mechanisms. PC12 cells were exposed to 100 μmol·L(-1) of H2O2 for 12 h with or without YGS40 pretreatment. Cytotoxicity was determined by MTT (3, (4, 5-dimethylthiazole-2-yl) 2, 5-diphenyl-tetrazolium bromide) and lactate dehydrogenase (LDH) release assays; apoptosis was detected by Annexin V/propidium iodide coupled staining and by determining caspase-3 activity and Bax and Bcl-2 protein levels. Mitochondrial membrane potential (MMP) was assessed by the retention of rhodamine123; and the activities of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured using commercially available enzymatic kits. Pretreatment with YGS40 significantly prevented H2O2-induced cytotoxicity and protected the cells against H2O2-triggered apoptosis characterized by externalization of membrane phosphatidylserine and caspase-3 activation and the increased ratio of Bax/Bcl-2 in PC12 cells. Further studies showed that YGS40 suppressed H2O2-induced MMP loss, increased SOD activity, and decreased MDA level. These findings suggest that YGS40 may be beneficial for the prevention and treatment of oxidative stress-mediated disorders.
