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Interactions between ginseng polysaccharides and ginsenosides in the anti‐cancer properties of American ginseng
Author(s) -
King Mandy L,
Selby Thomas D,
Murphy Laura L
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.717.6
Subject(s) - ginseng , ginsenoside , chemistry , apoptosis , polysaccharide , programmed cell death , cell cycle , herb , cytotoxic t cell , cancer cell , cell , traditional medicine , pharmacology , protein kinase b , microbiology and biotechnology , biochemistry , cancer , biology , medicine , medicinal herbs , in vitro , pathology , alternative medicine
Ginsenoside and polysaccharide extracts of the commonly used herb American ginseng have been shown to possess anticancer and immunostimulatory activity, respectively. Potential interactions between these components that may lead to the overall effect of ginseng have not been investigated. The aim of the current study was to determine the effects of conditioned media from RAW 264.7 peritoneal macrophages treated with ginsenoside fraction (GF‐CM), polysaccharide fraction (PS‐CM), or a combination of the two (GF+PS‐CM) on HT29 cancer cells. RAW 264.7 cells were treated for 24 hours with or without extracts and conditioned media was collected and analyzed for TNFα. HT29 cells were then treated with the conditioned media for 48 hours, counted, and analyzed for cell death, cell cycle distribution, or changes in protein expression. TNFα secretion was induced by PS in RAW 264.7 cells and this effect was attenuated in media collected from GF+PS treated macrophages. HT29 cells treated with PS‐CM showed decreased cell number, cell cycle arrest in G2/M, increased cell death, and increased expression of cleaved caspase‐3. Although GF‐CM treatment had no effects on HT29 cells, GF+PS‐CM resulted in inhibition of PS‐CM induced cell death and increased expression of phospho‐AKT. These results show that PS‐CM has a cytotoxic effect on HT29 cells and this effect is blocked by GF‐CM possibly through a mechanism involving AKT.