Effect of Sargassum fusiforme polysaccharide on apoptosis and its possible mechanism in human erythroleukemia cells.
10.1016/S1875-5364(20)60015-2
- Author:
Hao-Miao DING
1
,
2
;
Xue-Jia CHEN
3
;
Hai-Min CHEN
4
;
Cai-Sheng WANG
5
;
Guo-Ying QIAN
6
Author Information
1. School of Marine Sciences, Ningbo University, Ningbo 315211, China
2. College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China.
3. College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China.
4. School of Marine Sciences, Ningbo University, Ningbo 315211, China.
5. College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China. Electronic address: wangcaisheng@zwu.edu.cn.
6. College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China. Electronic address: qiangy@zwu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cell cycle;
Human erythroleukemia (HEL cells);
Polysaccharides;
Sargassum fusiforme
- From:
Chinese Journal of Natural Medicines (English Ed.)
2020;18(10):749-759
- CountryChina
- Language:English
-
Abstract:
This study aimed to investigate the effects of Sargassum fusiforme polysaccharide (SFPS I, II, and III) on the apoptosis and regulation of human erythroleukemia (HEL) cells. The effect of different doses of SFPS on HEL cell growth was detected using the Cell Counting Kit-8 method, and apoptosis was detected by Hoechst staining. Cell cycle distribution and apoptosis were detected using flow cytometry. Expression of the cell cycle gene, p53, antiapoptotic genes, Bcl-xL and Bcl-2, and pro-apoptotic genes, Bax, Bad, and Caspase-3, as well as the expression of the corresponding proteins, were detected using real-time quantitative polymerase chain reaction (qPCR) and Western blot. The results showed that SFPS II and III decreased HEL cell viability and induced HEL cell apoptosis. Different concentrations of SFPS (I, II, and III) were detected that induced much less toxic effect in normal human embryonic lung (MRC-5) cells, and SFPS I increased cell proliferation, indicating its favorable selectivity towards cancer cells. The mechanism by which SFPS induced apoptosis was also found to be related to the induction of cell cycle arrest in the G/G phase and the increased expression of apoptosis-related genes and proteins. We concluded that SFPS induces HEL cell apoptosis, possibly via activation of the Caspase pathway, providing the theoretical basis for the development of SFPS-based anti-tumor drug products.
