动物造模 z-bio 2022-02-10 400

　　Objective To investigate the inhibitory effect and anti-angiogenesis mechanism of gentiopicroside on H22 liver cancer mice.

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

　　Results Compared with the H22 liver cancer model group, the body weight of the 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). 30. 43% and 42. 93%; compared with the H22 liver cancer model group, the thymus index, spleen index and serum IFN-γ and IL-2 contents of mice in the low and high dose gentiopicroside groups were significantly increased (P<0 . 05 or P < 0. 01), while the expression of bFGF, TGF-β, VEGF, p-PI3K and p-Akt in tumor tissue was significantly decreased (P < 0. 05 or P < 0. 01).

　　Conclusion Gentiopicroside has inhibitory effect on tumor growth and angiogenesis in H22 liver cancer mice, which is related to improving immunity, increasing serum IFN-γ and IL-2 levels and inhibiting the activation of PI3K/Akt signaling pathway.