Hepatic arterial administration of ginsenoside Rg3 and transcatheter arterial embolization for the treatment of VX2 liver carcinomas

Ginsenoside Rg3 has been demonstrated to inhibit tumor cell proliferation and angiogenesis. However, its effect on liver tumors when administered via the hepatic artery has not been investigated. The purpose of this study was to evaluate the therapeutic effect of hepatic artery administration of Rg3 combined with transcatheter arterial embolization (TAE) in the treatment of liver tumors. A total of 48 rabbits with VX2 liver tumors were randomly divided into four groups: Group 1, Rg3; Group 2, TAE; Group 3, Rg3 and TAE; and Group 4, control. Abdominal contrast computed tomography (CT) scans were performed 2 weeks before and after intervention to assess tumor growth. Immunohistochemical staining was used to detect the expression of the angiogenesis biomarkers CD31 and VEGF, and the cell apoptosis marker caspase-3. Semi-quantitative RT-PCR and western blotting were employed to detect the expression of the caspase-3, Bax and Bcl-2 apoptosis-related genes and proteins. In addition, HepG2 cells were treated with Rg3 at different concentrations (0, 25, 50, 75 and 100 mg/l) in vitro. An MTT assay and western blot analysis were used to analyze the cell proliferation and VEGF expression. Compared with the other experimental groups, the Rg3 and TAE group expressed significantly lower levels of CD31 and VEGF (P<0.05), significantly increased levels of the pro-apoptotic genes caspase-3 and Bax (P<0.05), and significantly reduced levels of anti-apoptotic Bcl-2 at the mRNA and protein levels (P<0.05). In vitro, Rg3 inhibited HepG2 cell proliferation and downregulated VEGF expression significantly. These results indicated that ginsenoside Rg3 combined with TAE may effectively inhibit tumor growth by inhibiting tumor angiogenesis and inducing cancer cell apoptosis.