Rehmannia glutinosa polysaccharide induced an anti-cancer effect by activating natural killer cells

Int J Biol Macromol. 2017 Dec;105(Pt 1):680-685. doi: 10.1016/j.ijbiomac.2017.07.090. Epub 2017 Jul 15.


Rehmannia glutinosa polysaccharide (RGP) has exhibited an immune stimulatory effect, such as dendritic cell activation, but it has not been studied in terms of the activation capacity of natural killer (NK) cells in mice in vivo. In this study, we examined the effect of RGP on the proliferation and activation of NK cells in the spleen, mesenteric lymph node (mLN), and blood in vivo and compared that function with that of Escherichia coli lipopolysaccharide. The administration of RGP to C57BL/6 mice induced the increase in circulating blood NK cell numbers and in the proliferation of NK cells in the spleen, mLN, and blood. Moreover, RGP treatment promoted the toll-like receptor-4-dependent production of interferon-gamma and the up-regulation of CD69 expression in spleen NK cells. RGP-treated NK cells enhanced the cytotoxic activity with type I IFN production against target Yac-1 cells. Finally, RGP treatment inhibited the CT26 tumor growth in the lung. These findings demonstrated that RGP promoted the activation of NK cells and inhibited tumor growth in mice in vivo.

Keywords: Anti-cancer; Cytotoxic effect; IFN-γ; Natural killer cells; Rehmannia glutinosa polysaccharide.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cytokines / metabolism
  • Intracellular Space / drug effects
  • Intracellular Space / metabolism
  • Killer Cells, Natural / cytology
  • Killer Cells, Natural / drug effects*
  • Killer Cells, Natural / immunology*
  • Lymphocyte Activation / drug effects*
  • Mice
  • Mice, Inbred C57BL
  • Polysaccharides / pharmacology*
  • Rehmannia / chemistry*
  • Spleen / immunology
  • Toll-Like Receptor 4 / metabolism
  • Xenograft Model Antitumor Assays


  • Antineoplastic Agents
  • Cytokines
  • Polysaccharides
  • Toll-Like Receptor 4