Enhancement of amygdalin activated with β-D-glucosidase on HepG2 cells proliferation and apoptosis

Carbohydr Polym. 2012 Sep 1;90(1):516-23. doi: 10.1016/j.carbpol.2012.05.073. Epub 2012 May 28.


The growth inhibition and induction of apoptosis brought by amygdalin and activated with β-D-glucosidase were tested for cytoactivity in HepG2 cells. The MTT viability assay showed that all samples had effects on HepG2 proliferation in dose and time response manners. IC50 of stand-alone amygdalin and activation with β-D-glucosidase on the proliferation of HepG2 cells for 48 h were 458.10 mg/mL and 3.2 mg/mL, respectively. Moreover, apoptotic cells were determined by AO/EB (acridine orange/ethidium bromide) fluorescent staining method and Annexin V-FITC/PI staining flow cytometry cell cycle analysis. With increasing of amygdalin concentration and the incubation time, the apoptotic rate was heightened. Compared with the control, there was significant difference (p<0.01). Together, these findings indicate that amygdalin had no strong anti-HepG2 activity; however the ingredients of amygdalin activated with β-D-glucosidase had a higher and efficient anti-HepG2 activity. It was therefore suggested that this combination strategy may be applicable for treating tumors with a higher activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amygdalin / chemistry*
  • Amygdalin / pharmacology
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Cell Proliferation / drug effects*
  • Cell Proliferation / physiology
  • Hep G2 Cells
  • Humans
  • beta-Glucosidase / chemistry*
  • beta-Glucosidase / pharmacology


  • Amygdalin
  • beta-Glucosidase