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Ginseng marc-derived low-molecular weight oligosaccharide inhibits the growth of skin melanoma cells via activation of RAW264.7 cells

Authors :
Jae Yeon Lee
Jeong Yeon Seo
Yong Il Park
Jisun Lee
Chang Won Lee
Doo Jin Choi
Source :
International Immunopharmacology. 29:344-353
Publication Year :
2015
Publisher :
Elsevier BV, 2015.

Abstract

Panax ginseng C.A. Meyer has been traditionally consumed to prevent or treat various medical disorders due to its diverse health benefits. Polysaccharides isolated from Panax ginseng have been known to possess various pharmacological activities, including immune modulating, anti-diabetic, and anti-obesity properties. Despite the increasing number of reports on the bioactivities of ginseng polysaccharides, little is known regarding the medicinal potential of ginseng-derived oligosaccharides. In this study, we prepared a lower-molecular weight oligosaccharide (GOS, MW. 2.2kDa) from ginseng polysaccharides (MW. 11-605kDa) by enzymatic degradation and evaluated for its immunostimulating activities in RAW 264.7 murine macrophage cells. GOS was shown to be a glucan type oligosaccharide mainly containing glucose residues (97.48 in molar %). Treatment with GOS (100-500μg/ml) dose-dependently enhanced the production of TNF-α, IL-6, and NO in RAW 264.7 cells. Western blot analysis indicated that GOS dose-dependently induced the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), p38, and nuclear factor κB (NFκB), which are upstream signalling molecules for cytokine production. While GOS was not cytotoxic to the RAW 264.7 macrophage cells at the concentration tested (up to 1000μg/ml), when B16F10 melanoma cells were co-cultured with the GOS-activated macrophages, the cell viability of melanoma cells was dose-dependently decreased through the induction of apoptotic cell death. Taken together, these results suggested that ginseng marc-derived GOS has anti-cancer activity in vitro against melanoma cells by potentiating macrophage function.

Details

ISSN :
15675769
Volume :
29
Database :
OpenAIRE
Journal :
International Immunopharmacology
Accession number :
edsair.doi.dedup.....466e4ed1a4d67577c88911c975b66adb
Full Text :
https://doi.org/10.1016/j.intimp.2015.10.031