论文部分内容阅读
[目的]研究大黄素对血管内皮生长因子(VEGF)受体(VEGFR)阻断作用及对结肠癌细胞抑制作用的机制。[方法]软琼脂集落实验法,流式细胞术检测大黄素对结肠癌细胞增殖和凋亡的影响;酪氨酸激酶活性分析,Western blot方法检测大黄素对VEGFR的抑制作用。[结果]大黄素抑制结肠癌细胞生长,引起细胞凋亡,凋亡率由对照组(0μmol/L)的(8.1±2.7)%上升至大黄素40μmol/L时的(27.8±10.9)%(P<0.01),呈浓度依赖性。大黄素抑制VEGFR酪氨酸激酶活性,VEGFR-1相对活性由对照组的100%降至大黄素40μmol/L时的22.4%(P<0.01),VEGFR-2降至58.5%(P<0.01),VEGFR-3降至31.6%(P<0.01),大黄素作用后,VEGFR酪氨酸磷酸化状态蛋白量减少。[结论]大黄素能够通过抑制VEGFR酪氨酸激酶活性而抑制结肠癌生长,可作为一种有效的肿瘤血管生成抑制剂。
[Objective] To investigate the mechanism of emodin on vascular endothelial growth factor (VEGF) receptor (VEGFR) blocking and its inhibitory effect on colon cancer cells. [Method] The soft agar colony assay was used to detect the effect of emodin on the proliferation and apoptosis of colon cancer cells by flow cytometry. The tyrosine kinase activity assay and the Western blot were used to detect the inhibitory effect of emodin on VEGFR. [Result] Emodin could inhibit the growth of colon cancer cells and cause apoptosis. The apoptosis rate of emodin increased from (8.1 ± 2.7)% of control group (0μmol / L) to (27.8 ± 10.9)% of emodin 40μmol / L P <0.01), in a concentration-dependent manner. Emodin inhibited the activity of VEGFR tyrosine kinase, the relative activity of VEGFR-1 decreased from 100% in the control group to 22.4% (P <0.01) in emodin 40μmol / L and decreased to 58.5% (P <0.01) , And VEGFR-3 decreased to 31.6% (P <0.01). After emodin treatment, the protein content of VEGFR tyrosine phosphorylation decreased. [Conclusion] Emodin can inhibit the growth of colon cancer by inhibiting the activity of VEGFR tyrosine kinase and can be used as an effective tumor angiogenesis inhibitor.