Fucoidan by inhibiting cathepsin D activities alleviates PC12 apoptosis induced by hydrogen peroxide.
- Author:
Ganlin ZHANG
1
;
Ping LI
;
Yujie LI
;
Xin LIU
;
Ying CHEN
;
Xiaogang WENG
;
Qing YANG
;
Xiaoxin ZHU
Author Information
1. School of Chinese Pharmacy, Beijing University of Chinese Medicine, Beijing 100102, China.
- Publication Type:Journal Article
- MeSH:
Alzheimer Disease;
drug therapy;
metabolism;
Animals;
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Caspase Inhibitors;
Cathepsin D;
antagonists & inhibitors;
metabolism;
Cell Line, Tumor;
Cell Survival;
drug effects;
Humans;
Hydrogen Peroxide;
metabolism;
Oxidative Stress;
drug effects;
PC12 Cells;
Polysaccharides;
pharmacology;
Rats
- From:
China Journal of Chinese Materia Medica
2011;36(8):1083-1086
- CountryChina
- Language:Chinese
-
Abstract:
Cathepisn D plays a key role in early process of apoptosis before mitochondrion damage and caspases activations, and also involves in Alzheimer's disease (AD). Glycosaminoglycans (GAGs) have been suggested to inhibit the progress of apoptosis. Fucoidan, a nature GAGs mimetic, is shown as a potential candidate for neuroregressive disease. Here we reported PC12 cells response to oxidative stress with clear cathepsin D release, followed by caspase-3 activation. We found that fucoidan treatment can alleviate cathepsin D and caspase-3 activation, and improve cell survival. Furthermore, for the first time, fucoidan was shown to directly inhibit human liver cathepsin D by a dose-dependent way. These results support that cathepsin D involves in early apoptosis, suggest that fucoidan can decrease apoptosis at lysosome-cathepsin D level, which opens a new therapeutic approach to AD.
