内皮抑素对子宫内膜癌HEC1B细胞凋亡及其机制研究

发布时间：2018-02-10 21:39

本文关键词： 内皮抑素子宫内膜癌凋亡聚腺苷二磷酸核糖聚合酶- 胱天蛋白酶-　出处：《中国临床药理学杂志》2017年20期 　论文类型：期刊论文

【摘要】：目的研究内皮抑素对子宫内膜癌HEC1B细胞增殖、凋亡及其对聚腺苷二磷酸核糖聚合酶-1(PARP-1)和胱天蛋白酶-3(Caspase-3)表达的影响。方法用终浓度为10,50,100,200 mmol·L~(-1)的内皮抑素干预的子宫内膜癌HEC1B细胞为实验组,无任何药物处理的子宫内膜癌HEC1B细胞为对照组。培养48,72 h后,用噻唑蓝(MTT)比色法检测各组子宫内膜癌HEC1B细胞增殖情况。用Hoechst33258荧光染色法检测子宫内膜癌HEC1B细胞凋亡情况;用酶联免疫吸附(ELISA)法检测子宫内膜癌HEC1B细胞培养上清液中PARP-1和Caspase-3表达情况。结果对照组48,72 h细胞增殖抑制率分别为(6.24±0.39)%,(5.63±0.41)%,10,50,100,200 mmol·L~(-1)实验组48 h细胞增殖抑制率分别为(6.98±0.52)%,(14.36±1.02)%,(24.31±2.06)%,(28.16±2.13)%;10,50,100,200 mmol·L~(-1)实验组72 h细胞增殖抑制率分别为(8.96±0.54)%,(23.16±2.45)%,(29.48±2.81)%,(38.49±0.68)%。与对照组比较,10,50,100,200 mmol·L~(-1)实验组不同培养时间HEC1B细胞的增殖抑制率均显著升高(P0.01),且HEC1B细胞的增殖抑制率随着培养时间的延长及药物浓度的增加而增大(P0.05或P0.01)。内皮抑素干预子宫内膜癌HEC1B细胞72 h后,荧光染色可见,与对照组比较,实验组细胞出现细胞核固缩、细胞核碎裂、凋亡小体形成及荧光强度增强等凋亡特征。10,50,100,200 mmol·L~(-1)实验组子宫内膜癌HEC1B细胞培养上清中PARP-1蛋白表达量低于对照组,Caspase-3蛋白表达量明显高于对照组(P0.05或P0.01),且呈现一定的浓度依赖性。结论内皮抑素可抑制子宫内膜癌HEC1B细胞的增殖,并促其凋亡,其机制可能与下调PARP-1表达及上调Caspase-3表达有关。
[Abstract]:Objective to study the effect of endostatin on the proliferation of HEC1B cells in endometrial carcinoma. Apoptosis and its effect on the expression of polyadenosine diphosphate polymerase 1 (PARP-1) and cystatin 3 (Caspase-3). Methods HEC1B cells of endometrial carcinoma were treated with endostatin at the final concentration of 1050 ~ 100 mmol 路L ~ (-1). HEC1B cells of endometrial carcinoma without any drug treatment were used as control group. After 48 hours of culture, the proliferation of endometrial carcinoma HEC1B cells was detected by MTT colorimetry, and the apoptosis of endometrial carcinoma HEC1B cells was detected by Hoechst33258 fluorescence staining. The expression of PARP-1 and Caspase-3 in the culture supernatant of endometrial carcinoma HEC1B cells was detected by Elisa. Results the cell proliferation inhibition rates in the control group were 6.24 卤0.397h, 5.63 卤0.41g / h, respectively. The inhibitory rates of proliferation in the experimental group were 6.98 卤0.52h, 14.36 卤1.02g, 24.31 卤2.06g / h, 28.16 卤2.1300200 mmol 路L ~ (-1), respectively.The inhibitory rates of cell proliferation in the experimental group were 14.36 卤1.02 卤24.31 卤2.06 ~ 28.16 卤2.13100 mmol 路L ~ (-1), respectively. The inhibitory rates of proliferation of HEC1B cells in the experimental group at 72 h were 8.96 卤0.54 and 23.16 卤2.45 and 29.48 卤2.81, respectively. Compared with the control group, the inhibitory rates of proliferation of HEC1B cells in the experimental group were significantly higher than those in the control group, and the inhibition rate of HEC1B cells increased with the prolongation of the culture time and the concentration of drugs. After 72 h of endostatin intervention on HEC1B cells of endometrial carcinoma, Fluorescence staining showed that compared with the control group, the cells in the experimental group showed pyknosis and fragmentation. The expression of PARP-1 protein in the supernatant of HEC1B cell culture of endometrial carcinoma in the experimental group was lower than that in the control group (P0.05 or P0.01), and the expression of PARP-1 protein in the culture supernatant of endometrial carcinoma cells in the experimental group was significantly higher than that in the control group (P0.05 or P0.01A), and the expression of PARP-1 protein in the culture supernatant of endometrial carcinoma cells in the experimental group was significantly higher than that in the control group. Conclusion endostatin can inhibit the proliferation of HEC1B cells in endometrial carcinoma. The mechanism may be related to down-regulation of PARP-1 expression and up-regulation of Caspase-3 expression.
【作者单位】：安徽医科大学附属省立医院妇产科;
【基金】：安徽省教育厅高校自然科学研究基金资助项目(KJ2016A482)
【分类号】：R737.33

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