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Carbohydr Polym ; 95(1): 282-7, 2013 Jun 05.
Article in English | MEDLINE | ID: mdl-23618270

ABSTRACT

Sulfated polysaccharides have been known to inhibit proliferation in tumor cells. However, the molecular mechanisms involved in sulfated polysaccharides-induced apoptosis are still uncharacterized. In this study, the effect of a chemically sulfated polysaccharide obtained from Grifola frondosa (S-GFB) on HepG2 cell proliferation and apoptosis-related mechanism were investigated. It was found that S-GFB inhibited proliferation of HepG2 cells in a dose-dependent manner with IC50 at 48 h of 61 µg ml(-1). The results of scanning electron micrographs indicated that S-GFB induced typical apoptotic morphological feature in HepG2 cells. Flow cytometric analysis demonstrated that S-GFB caused apoptosis of HepG2 cells through cells arrested at S phase. Western-blotting results showed that S-GFB inhibited notch1 expression, IκB-α degradation and NF-κB/p65 translocation from cytoplasm into nucleus. Simultaneously, the apoptotic mechanism of HepG2 cells induced by S-GFB was associated with down regulation of FLIP, and activation of caspase-3 and caspase-8. Taken together, these findings suggest that the S-GFB induces apoptosis through a notch1/NF-κB/p65-mediated caspase pathway.


Subject(s)
Grifola , Polysaccharides/pharmacology , Receptor, Notch1/metabolism , Transcription Factor RelA/metabolism , Apoptosis/drug effects , CASP8 and FADD-Like Apoptosis Regulating Protein/metabolism , Caspase 3/metabolism , Caspase 8/metabolism , Cell Survival/drug effects , Hep G2 Cells , Humans , Polysaccharides/chemistry , Signal Transduction/drug effects
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