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Ming Y.-L.,Research and Development Center for Medicine Plant and Plant Drugs | Zheng Z.-Z.,Research and Development Center for Medicine Plant and Plant Drugs | Chen L.-H.,Research and Development Center for Medicine Plant and Plant Drugs | Tong Q.-X.,Research and Development Center for Medicine Plant and Plant Drugs
Chinese Traditional and Herbal Drugs | Year: 2010

Objective: In order to investigate the sensitization of 20-O-β-D-glucopyranoside-20(S)-protopanaxadiol (ginsenoside IH901) with several common drugs CTX, 5-FU, cDDP in hepatocellular carcinoma (HCC) Bel-7402 and SMMC-7721. Methods: The inhibitory rates on HCC in IH901, CTX, 5-FU, cDDP, IH901 with CTX, IH901 with 5-FU, and IH901 with cDDP groups were detected by MTT assay. The synergism index, Q value, was calculated to judge the sensitization of combined drugs. Results: The IH901 with CTX group could increase the inhibitory effect on cell proliferation of HCC significantly with the synergistic effect. The inhibitory rate in IH901 with 5-FU group was just superposition on two cell lines. IH901 with cDDP group was still superposition on Bel-7402, but lightly had the synergistic effect on SMMC-7721. Conclusion: The IH901 could increase the inhibitory effect of CTX on cell proliferation of HCC and the sensitizasion on chemotherapy and also have wide adaptability. Source


Zheng Z.-Z.,Research and Development Center for Medicine Plant and Plant Drugs | Ming Y.-L.,Research and Development Center for Medicine Plant and Plant Drugs | Ming Y.-L.,Xiamen University | Chen L.-H.,Research and Development Center for Medicine Plant and Plant Drugs | And 4 more authors.
Oncology Reports | Year: 2014

An intestinal bacterial metabolite of ginseng protopanaxadiol saponin, 20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol (compound K), has been reported to induce apoptosis in a variety of cancer cells. However, the precise mechanisms induced by compound K in human hepatocellular carcinoma (HCC) cells remain unclear. In order to examine possible apoptotic mechanisms, we investigated the anticancer effect of compound K in MHCC97-H. MTT assay showed that compound K inhibited the proliferation of MHCC97-H cells with a relatively low toxicity in normal hepatoma cells. Cell cycle progression and cell staining showed an increase in apoptotic sub-G1 fraction. Treatment of MHCC97-H with compound K also induced a reduction in mitochondrial membrane potential (Δψm) and DNA damage. Further study showed that compound K upregulated Fas, FasL, Bax/Bcl-2 ratio and downregulated pro-caspase-9, pro-caspase-3 in a dose-dependent manner, and it also inhibited Akt phosphorylation. These results suggest that compound K significantly inhibits cell proliferation and induces apoptosis in MHCC97-H cells through Fas- and mitochondria-mediated caspase-dependent pathways in human HCC cells. Source

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