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Stereospecificity of Ginsenoside Rg3 in the Promotion of Cellular Immunity in Hepatoma H22‐Bearing Mice
Author(s) -
Wu Rihui,
Ru Qin,
Chen Lin,
Ma Baomiao,
Li Chaoying
Publication year - 2014
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.12518
Subject(s) - in vivo , ginsenoside , immune system , chemistry , immunity , pharmacology , stimulation , in vitro , cellular immunity , interferon , cancer research , immunology , medicine , biology , biochemistry , ginseng , alternative medicine , microbiology and biotechnology , pathology
Previous investigations have demonstrated that ginsenoside Rg3 (Rg3) has many actions including antitumor, antioxidative, and immunomodulatory effects. However, Rg3 exists as 2 stereoisomeric pairs, 20(S)‐ginsenoside Rg3 [20(S)‐Rg3] and 20(R)‐ginsenoside Rg3 [20(R)‐Rg3], which have disparate pharmacological actions because of their different chemical structures. In this study, the 2 epimers were compared for their effects on the growth of hepatocellular carcinoma H22 transplanted tumors and the immune function of H22‐bearing mice. In vivo efficacy study showed that the growth of H22 transplanted tumors was significantly inhibited when treated with 20(S)‐Rg3 and 20(R)‐Rg3 ( P < 0.05), and the inhibition rate of tumor growth was 23.6% and 40.9%, respectively. Furthermore, the cellular immunity of H22‐bearing mice was remarkably enhanced after Rg3 treatment ( P < 0.05), which may be due to stimulation of ConA‐induced lymphocyte proliferation and augmentation of Th1‐type cytokines interleukin‐2 and interferon‐γ levels in mice. Interestingly, the effects of 20(R)‐Rg3 were significantly greater than those of the S‐form ( P < 0.05). Taken together, these results indicate that Rg3 inhibits H22 tumor growth in vivo at least partly by improving the host's cellular immunity in a stereospecific manner, and 20(R)‐Rg3 is more potent for treating cancers or other immune‐mediated diseases clinically.