【摘要】 目的探讨水飞蓟宾抑制缺氧状态下胃癌细胞MGC803细胞的生长增殖的分子机制。方法体外缺氧条件下体外培养胃癌细胞系MGC803,用不同浓度水飞蓟宾处理后,采用MTT检测水飞蓟宾对MGC803细胞增殖的影响,Western blot检测Akt的磷酸化。酶联免疫吸附试验(ELISA)检测血管内皮生长因子(VEGF)的分泌情况。结果 0~250μmol/L蓟宾可显著抑制胃癌细胞MGC803增殖,但0~100μmol/L水飞蓟宾对Akt磷酸化以及VEGF分泌无明显影响,而250μmol/L水飞蓟宾可诱导MGC803细胞磷酸化并抑制VEGF分泌。结论水飞蓟宾可能通过影响PI3K/Akt磷酸化以及VEGF的分泌而发挥抗肿瘤活性。更多还原

【Abstract】 Objective To observe the molecular mechanism of stomach cancer cell line MGC803 proliferation in the state of hypoxia ihibited by silibinin. Methods Stomach cancer cell line MGC803 was cultured in vitro in the condition of hypoxia in vitro, the effect of silibinin on MGC803 proliferation was detected by MTT after different concentrations of silibinin treatment, the phosphorylation of Akt was detected by Western blot, the secretion situations of vascular endothelial growth factors were detected by enzyme linked immunosorbent assay. Results 0-250μmol/L silibinin could obviously inhibit stomach cancer cell line MGC803 proliferation, but 0-100μmol/L silibinin had no obvious effect on phosphorylation of Akt and VEGF secretion, and 250μmol/L silibinin could induce the phosphorylation of MGC803 cells and inhibit VEGF secretion.Conclusion Silibinin may exert its anti-tumor activity by influencing the phosphorylation of PI3K/Akt and VEGF secretion.更多还原