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为研究注射用胞必佳在体外诱导人肝癌细胞HepG2凋亡的作用与机制,采用MTT法和LDH法检测胞必佳对HepG2细胞的增殖抑制作用、细胞毒性作用;AO/EB双荧光染色观察细胞形态学变化;流式细胞术检测细胞周期分布。结果显示,胞必佳作用HepG2细胞后,呈浓度依赖性抑制HepG2细胞的生长,作用24,48,72 h IC50分别为:187.53,155.31,92.54μg/mL;胞必佳对HepG2细胞24,48 h的致死率达68%左右。AO/EB荧光染色可见细胞出现明显的凋亡形态学改变。不同浓度胞必佳对HepG2细胞周期的影响表现为G1期阻滞,G2/M期和S期细胞所占比例减小。胞必佳对HepG2细胞有明显的生长抑制作用,并诱导肿瘤细胞凋亡,其抗肿瘤作用的机理可能是:通过干扰细胞周期调控点,主要阻止G1期细胞向G2/M期的转变。
In order to study the effect and mechanism of BSP on human hepatocellular carcinoma cell HepG2 induced apoptosis in vitro, MTT assay and LDH assay were used to detect the inhibitory effect of BSP on HepG2 cell proliferation and cytotoxicity; AO / EB double fluorescent staining Cell morphological changes; flow cytometry to detect cell cycle distribution. The results showed that after the cells had good effect on HepG2 cells, the growth of HepG2 cells was inhibited in a concentration-dependent manner. The IC50 values at 24, 48 and 72 h were 187.53, 155.31 and 92.54 μg / mL, respectively. HepG2 cells 24, 48 h lethal rate of about 68%. AO / EB fluorescence staining showed obvious morphological changes of apoptotic cells. The effects of different concentrations of BPS on HepG2 cell cycle were arrested in G1 phase, and the proportion of cells in G2 / M phase and S phase decreased. Cell may have a good inhibitory effect on HepG2 cells and induce apoptosis of tumor cells. The mechanism of anti-tumor effect may be: by interrupting the cell cycle regulation point, mainly to prevent G1 phase cells to G2 / M phase transition.