Mechanism of apoptosis of nasopharyngeal carcinoma cells induced by polysaccharides extracts from Hedyotic diffusa.
- Author:
JING YAN
;
KANG MIN
;
LIU JIN
;
LI JINGYU
;
TANG ANZHOU
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Carcinoma;
Caspase 3;
metabolism;
Cell Line, Tumor;
drug effects;
Cell Proliferation;
Down-Regulation;
Hedyotis;
chemistry;
Humans;
Nasopharyngeal Carcinoma;
Nasopharyngeal Neoplasms;
pathology;
Plant Extracts;
pharmacology;
Polysaccharides;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2015;29(7):641-644
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the proliferation inhibition and apoptosis of polysaccharides extracts from polysaccharides extracts from Hedyotic diffusa (PEHD) on Human Nasopharyngeal Carcinoma (NPC)cell line CNE2 cells in vitro.
METHOD:CNE2 cells treated with various concentrations of PEHD were detected by MTT assay at 24 h, 48 h, and 72 h. The apoptotic cells were analyzed by flow cytometry with Annexin V/PI staining. The expression levels of Bax, Bcl-2 and caspase-3 protein were examined by Western blotting method.
RESULT:The growth of CNE2 cells were suppressed after treatment with PEHD (P < 0.05), MTT assay showed that the highest cell inhibition rate reached to 76.5%, the inhibition in the doses from 2 to 6 mg/ml showed dose-and-time-dependent. The percent of apoptosis in 4 and 6 mg/ml PEHD treatment groups for 48 h were 31.32%, 46.28%, respectively, and significantly higher than that in control groups, 4.86% (P < 0.01). After the cells being treated with PEHD for 48 h, the expression of Bax and caspase-3 protein increased, and the expression of Bcl-2 protein decreased gradually.
CONCLUSION:PEHD could inhibited the growth of CNE2 cells and was dose-and-time-dependent, the mechanism may involve induction of cell apoptosis, which was associated with the activation of Bax and caspase-3 protein and the down-regulation of Bcl-2 protein expression.