Purpose: To study the effect of 3,3′-biisofraxidin from
Sarcandrae Herba
on the proliferation of BGC-
823 cells and the possible mechanisms.
Methods: Cell Counting Kit-8 (CCK-8), flow cytometry, Western blot and xenograft assays were used to
determine the effects of 3,3′-biisofraxidin on the proliferation, apoptosis, apoptotic proteins and
xenograft of BGC-823 cells.
Results: 3,3′-Biisofraxidin significantly (p < 0.01) inhibited the proliferation of BGC-823 cells
(concentrations: 10 - 40 μM; cell viability: 30.45 - 76.68 % in CCK-8 assay) with half maximal inhibitory
concentration (IC50) value of 20.35 μM and induced the apoptosis of BGC-823 cells (concentrations:
10, 20 and 40 μM; apoptotic cells: 11.92, 20.10 and 33.64 % in flow cytometry assay), compared with
the control (cell viability: 99.73 %; apoptotic cells: 5.18 %). 3,3′-Biisofraxidin (10, 20 and 40 μM in vitro;
40 mg/kg in vivo) significantly (p < 0.05 or 0.01) down-regulated the expressions of anti-apoptotic
proteins (Bcl-2, Bcl-xl and Survivin) and up-regulated the expressions of pro-apoptotic proteins (Smac,
caspase-3, caspase-7 and caspase-9), compared with the control. Moreover, the release of cytochrome
c from the mitochondria to the cytoplasm was significantly (p < 0.01) promoted in vitro, compared with
the control. 3,3′-Biisofraxidin (40 mg/kg) significantly (p < 0.05 or 0.01) inhibited the growth of tumor in
xenograft assay, compared with the control.
Conclusion: 3,3′-Biisofraxidin significantly induces the apoptosis of BGC-823 cells in vitro and in vivo
through the mitochondria-mediated apoptotic pathway, and therefore has a potential to be developed
into an anti-gastric cancer drug.