中文摘要：

目的：探讨碳纳米管（CNT）-树形分子递送Survivin反义寡核苷酸（ASOND）进入肝癌细胞HepG2的效率及其对肝癌细胞增殖的影响。方法：制备碳纳米管与PAMAM树形分子复合物，与Survivin反义寡核苷酸组装后，用原子力显微镜（AFM）与凝胶电泳观察碳纳米管-树形分子-反义核苷酸复合物的形态结构；然后将复合物与人肝癌HepG2细胞共培养，同时设立对照，采用透射电镜观察碳纳米管-树形分子-反义核苷酸复合物在细胞中的定位，采用MTT法检测复合物对癌细胞生长的抑制作用。结果：AFM与凝胶电泳分析证实碳纳米管-树形分子-反义核苷酸复合物被成功制备。透射电镜观察证实碳纳米管-树形分子-反义核苷酸复合物位于细胞质。MTT法检测表明，CNT-PAMAM-ASODN浓度为1．0 μmol／L时，即可抑制（45．97±4．28）％的HepG2细胞增殖，而ASODN组和CNT-PAMAM组在此浓度条件下对HepG2细胞的抑制率则分别为（9．33±0．85）％和（6．37±0．69）％；当CNT-PAMAM-ASODN达到1．50 μmol／L时，细胞抑制率为（70．22±7．25）％，而且抑制作用随培养时间的延长与浓度的增加而增强，实验组与对照组之间细胞抑制率存在显著性差异（P＜0．01）。结论：碳纳米管一树形分子复合物是一种高效的基因递送载体，能够携带Survivin反义寡核苷酸进入肝癌细胞，并高效抑制HepG2细胞的增殖，显著增强反义寡核苷酸的作用效果。

英文摘要：

Objective： To investigate the efficiency of carbon nanotube（CNT） -PAMAM mediated entrance of anti-survivin oligonucleotide into HepG2 cells, and its effects on the proliferation of HepG2 cells. Methods： CNT-PAMAM-antisurvivin oligonucleotide compounds were prepared and characterized by AFM and 1% agarose gel electrophoresis analysis. TEM was used to observe the distribution of CNT-PAMAM-ASODN compounds in HepG2 cells. CNT-PAMAM-ASODN compounds were added into the medium and co-cultured with HepG2 cells for 24 h, 48 h,72 h, and 96 h at 37℃, 5% CO2. MTT method was used to detect the effects of ASODN and CNT-PAMAM-ASODN on the proliferation of HepG2 cells. Results： CNT-PAMAM-ASODN compounds were successfully synthesized via AFM and agarose gel electrophoresis. TEM showed that the compounds were located in the cytoplasm. When CNT-PAMAM-ASODN （ 1.0 μmol/L） and ASODN （1.0 μmol/L） were used for a 48 h culture, the inhibitory rates of HepG2 cells were （45.97 ±4.28 ） % for CNT-PAMAM-ASODN compounds group, （9.33 ± 0.85 ） % for ASODN group, and （ 6.37 ± 0.69） % for CNT-PAMAM group. CNT-PAMAM-ASODN compounds at 1.5 μmol/L inhibited HepG2 cells by （70.22 ± 7.25 ） %, and the inhibitory effects were in a time- and concentration-dependent manner. There was statistical difference between experiment group and control group （ P 〈 0.01 ）. Conclusion ： CNT-PAMAM compounds may serve as a gene delivery vector with high efficiency, which can bring survivin ASODN into HepG2 cells, inhibiting HepG2 cell proliferation and markedly enhancing the inhibitory effects of survivin against HepG2 cells.