论文部分内容阅读
目的分析含RGD序列的多肽ERC(N5)与整合素αVβ3结合的能力,并探讨其对肝癌HepG2细胞增殖与凋亡的影响。方法利用流式细胞术检测HepG2细胞表面整合素αVβ3的含量以及ERC(N5)与FITC-αVβ3抗体LM609竞争结合HepG2细胞的情况;用ERC(N5)处理HepG2细胞,CCK-8法检测细胞增殖活力,光学显微镜下观察细胞形态变化,流式细胞术分析细胞凋亡率。结果 HepG2细胞表面αVβ3的含量为47.0%;浓度为8、16、32和64μmol/L的ERC(N5)均能抑制LM609与HepG2细胞的结合及细胞的增殖活力,且呈剂量依赖性(P<0.05);与对照组相比,经16μmol/L ERC(N5)处理的细胞可见形态发生明显改变,细胞凋亡率明显升高。结论 ERC(N5)可特异结合整合素αVβ3,并通过抑制αVβ3的作用来抑制肝癌HepG2细胞增殖,并诱导细胞凋亡。
Objective To analyze the ability of ERC (N5) containing RGD sequence to bind integrin αVβ3 and investigate its effect on proliferation and apoptosis of HepG2 cells. Methods Flow cytometry was used to detect the content of integrin αVβ3 on HepG2 cells and the competition of ERC (N5) with HepG2 cells by FITC-αVβ3 antibody LM609. HepG2 cells were treated with ERC (N5) The morphological changes of the cells were observed under a light microscope, and the apoptosis rate was analyzed by flow cytometry. Results The concentration of αVβ3 on HepG2 cells was 47.0%. ERCs (N5) at concentrations of 8, 16, 32 and 64 μmol / L all inhibited the binding of LM609 to HepG2 cells and the proliferation activity of HepG2 cells in a dose-dependent manner (P < 0.05). Compared with the control group, the morphological changes of the cells treated with 16μmol / L ERC (N5) showed obvious changes and the apoptosis rate was significantly increased. Conclusion ERC (N5) can specifically bind to integrin αVβ3 and inhibit the proliferation and induce apoptosis of HepG2 cells by inhibiting the effect of αVβ3.