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目的探讨环氧合酶-2(COX-2)反义寡核苷酸抑制Hela细胞增殖的机制及其临床意义。方法2004年5月至2005年5月在温州医学院附属一院将Hela细胞用MEM培养基培养,像差倒置显微镜下观察细胞的增殖情况。Hela细胞分4组培养:正常对照组、反义寡核苷酸(ASODNS)转染组、正义寡核苷酸(SODNS)转染组、脂质体处理组。细胞转染后48h,采用流式细胞仪检测各组细胞周期的变化。结果反义寡核苷酸转染组细胞的增殖受到了显著抑制,ASODNS处理的细胞与其它组比较,G2/M期细胞[(10.75±0.24)%]所占比例增高明显(P<0.05),S期细胞[(10.13±0.04)%]比例明显减少,差异有显著性意义(P<0.05),而G0/G1期[(79.12±0.06)%]无统计学意义的改变。结论ASODNS对Hela细胞的增殖具有抑制作用,其抑制机制可能与引起细胞周期再分布,降低S期细胞比例及阻滞细胞G2/M期有关。
Objective To investigate the mechanism of cyclooxygenase-2 (COX-2) antisense oligonucleotide on Hela cell proliferation and its clinical significance. Methods From May 2004 to May 2005, Hela cells were cultured in MEM medium in Wenzhou First Affiliated Hospital of Wenzhou Medical College. Cell proliferation was observed under an inverted phase contrast microscope. Hela cells were divided into 4 groups: normal control group, antisense oligonucleotide (ASODNS) transfection group, superantigen (SODNS) transfection group and liposome treatment group. 48h after transfection, the changes of cell cycle in each group were detected by flow cytometry. Results The proliferation of cells transfected with antisense oligodeoxynucleotides was significantly inhibited. Compared with other groups, the percentage of cells in G2 / M phase increased significantly (P <0.05) (10.13 ± 0.04)%] in S phase were significantly lower than those in control group (P <0.05), but there was no significant change in G0 / G1 phase [(79.12 ± 0.06)%]. Conclusion ASODNS can inhibit the proliferation of Hela cells. The mechanism may be related to the redistribution of cell cycle, the decrease of the proportion of S phase cells and the arrest of G2 / M phase.