QIN An-min, SI Ying-ming, FU Ying-ying, LIU Si-li. Study on the apoptosis induced by dihydromyricetin in human ovarian cancer HO-8910 cells and its mechanism[J]. Journal of Bengbu Medical University, 2021, 46(10): 1340-1345. DOI: 10.13898/j.cnki.issn.1000-2200.2021.10.004
    Citation: QIN An-min, SI Ying-ming, FU Ying-ying, LIU Si-li. Study on the apoptosis induced by dihydromyricetin in human ovarian cancer HO-8910 cells and its mechanism[J]. Journal of Bengbu Medical University, 2021, 46(10): 1340-1345. DOI: 10.13898/j.cnki.issn.1000-2200.2021.10.004

    Study on the apoptosis induced by dihydromyricetin in human ovarian cancer HO-8910 cells and its mechanism

    • ObjectiveTo investigate the effects of dihydromyricetin on the growth and apoptosis of human ovarian cancer HO-8910 cells, and its mechanism.
      MethodsThe HO-8910 cells were cultured in vitro, and treated with dihydromyricetin at different concentrations(10, 20 and 40 μmol/L).The proliferation of cells was detected using MTT and CCK-8 method, the apoptosis of cells was detected using the Annexin V-FITC/PI flow cytometry and Hoechst 33258 fluorescence staining, and the expression levels of Caspase-3, Bcl-2, Bax, ERK and p-ERK protein were detected using Western blotting.
      ResultsThe results of MTT and CCK-8 was showed that dihydromyricetin could inhibit the growth of HO-8910 cells in a concentration-dependent manner.The results of flow cytometry showed that dihydromyricetin could promote the HO-8910 cell apoptosis in a concentration-dependent manner.The typical morphological changes of apoptosis in HO-8910 cells treated with dihydromyrmectin were found using Hoechst 33258 fluorescence staining.The results of Western blotting showed that dihydromyricetin could up-regulate the levels of Caspase-3 and Bax, and down-regulate the levels of Bcl-2, ERK and p-ERK in HO-8910 cells(P < 0.05).
      ConclusionsDihydromyricetin can inhibit the activity of human ovarian cancer HO-8910 cells and induce their apoptosis, and the mechanism of which is related to the regulation of ERK/MAPK signaling pathway.
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