[Animal modeling] - Analysis of gentiopicrin on tumor growth inhibition and anti angiogenesis in H22 hepatoma mice

  Objective To investigate the inhibitory effect of gentiopicrin on tumor growth and anti angiogenesis mechanism in H22 hepatoma mice.

  Methods H22 liver cancer model was established by subcutaneous injection of H22 cell suspension into the right axilla of mice. The mice were randomly divided into model group, gentiopicroside low and high dose groups (50 mg/kg, 100 mg/kg) and cyclophosphamide group (20 mg/kg) with 10 mice in each group; Another 10 healthy mice were selected as the normal group; 14 days after administration, body weight, tumor weight, tumor inhibition rate, thymus index, spleen index and serum interferon were detected- γ (IFN- γ)、 Interleukin-2 (IL-2) content, basic fibroblast growth factor (bFGF) and transforming growth factor in tumor tissue- β (TGF- β)、 Expression levels of vascular endothelial growth factor (VEGF), phosphorylated phosphatidylinositol 3 kinase (p-PI3K) and phosphorylated protein kinase B (p-Akt).

  Results Compared with H22 liver cancer model group, the weight of mice in the low and high dose gentiopicroside groups did not change significantly (P>0.05), but the tumor weight decreased significantly (P<0.01), and the tumor inhibition rates were 30.43% and 42.93% respectively; Compared with H22 liver cancer model group, thymus index, spleen index and serum IFN of mice in low and high dose gentiopicroside groups- γ、 IL-2 content increased significantly (P<0.05 or P<0.01), while bFGF and TGF in tumor tissue- β、 The expression of VEGF, p-PI3K and p-Akt decreased significantly (P<0.05 or P<0.01).

  Conclusion Gentiopicrin can inhibit tumor growth and angiogenesis in H22 hepatoma mice, which is related to improving immunity and increasing serum IFN- γ、 IL-2 content is related to inhibition of PI3K/Akt signal pathway activation.