Anti-proliferative and cytoskeleton-disruptive effects of icariin on HepG2 cells.

Abstract

Several biological properties of icariin have been identified, including its anticancer effect. However, the potential mechanisms underlying the effect of icariin on HepG2 hepatocellular carcinoma cells remain to be elucidated. The aim of the present study was to examine the effects of icariin on the proliferation and cytoskeleton of HepG2 cells. A 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5 diphenyltetrazolium bromide assay was used to assess the antiproliferative effects of icariin and to determine the optimal concentration and treatment schedule of icariin on the HepG2 cells. Cell cycle analysis was performed using fluorescence activated cell sorting, the protein expression of B‑cell lymphoma (Bcl)‑2 was determined using immunohistochemical and western blot analyses, and F‑actin in the cells was examined using confocal microscopy. The chemotherapeutic drug, oxaliplatin, was used as a positive control. The results demonstrated that the optimal concentration of icarrin to produce an antiproliferative effect on HepG2 cells was 10‑5 mol/l, and the optimal treatment duration was 72 h. The icariin group had a significantly higher proportion of cells in the G0/G1 phase, compared with the control group, treated with high glucose Dulbecco's modified Eagles medium with 10% fetal bovine serum (P<0.05). The proportion of HepG2 cells in the S phase was significantly lower in the oxaliplatin (24.19%; P<0.05) and icariin (21.07%; P<0.01) groups, compared with the control group (28.62%). Icariin markedly decreased the expression of Bcl‑2, compared with the control (P<0.01), and disrupted the polymerization of F‑actin filaments in the HepG2 cells. Therefore, the present study demonstrated that, at an optimum concentration of 10‑5 mol/l, icariin inhibited the proliferation of the HepG2 cells, promoted apoptosis by decreasing the expression of Bcl‑2, and disrupted the actin cytoskeleton.