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染料木素对人宫颈癌细胞株HeLa增殖的影响 被引量:2

Effect of genistein on proliferation of human cervical cancer cell (HeLa)
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摘要 目的研究染料木素对人宫颈癌细胞株(HeLa)增殖的影响,并初步探讨其可能的作用机制。方法用无酚红DMEM高糖培养基(含10%活性炭处理过的胎牛血清)培养HeLa细胞,使用不同浓度染料木素(0.001~10μmol·L-1)作用,采用MTT法检测细胞增殖变化,流式细胞仪检测细胞周期及细胞凋亡的变化,Western blot检测雌激素受体ERα蛋白表达的变化。结果实验浓度区间的染料木素作用于HeLa细胞48、72 h后,均能促进HeLa细胞的增殖。在该浓度区间下,染料木素能够促进HeLa细胞由G1期进入S期,增加HeLa细胞S期细胞比例,减少G1期细胞比例;同时,细胞凋亡降低,ERα蛋白表达量提高。结论染料木素在0.001~10μmol·L-1浓度范围内能够刺激HeLa细胞增殖,这一增殖效果可能是通过上调ERα表达量、调节细胞周期及凋亡相关信号通路产生的。 Aim To investigate the effect of genistein on the proliferation of human cervical cancer cell ( HeLa) in vitro and discuss the possible mechanism. Methods HeLa cells were treated with genistein, whose concentration range was from 0. 001 to 10 μmol·L^-1. MTT assay was used to detect the amount of HeLa cells, which could reflect the change of their proliferation. Cell cycle and cell apoptosis were observed via flow cytometry. ERα expression was detected through Western blot. Results Compared with control group, all the experimental concentrations could promote the proliferation of HeLa cells after the cultivation with genistein for 48 h and 72 h. Within the concentrations, genistein could promote HelJa cells in G1 phase entering S phase, which could increase the proportion of cells in S phase and decrease cell proportion in G1 phase. Meanwhile, a significant decrease of the proportion of apoptosis was observed, which was in accordenee with the cell cycle test. Moreover, compared with control group, the expression of ERα protein was significantly higher after the cultivation with genistein for 6 h and 12 h. Conclusion Genistein (0. 001 -10 μmol·L^-1) can stimulate HeLa cells proliferation, which might through enhancing the expression of ERα and influeneing the signal pathway related to cell cycle and apoptosis.
出处 《中国药理学通报》 CAS CSCD 北大核心 2013年第11期1577-1581,共5页 Chinese Pharmacological Bulletin
基金 科技部国际科技合作计划项目(No 2010DFA31780) 国家基金委中德科学基金项目(No GZ731)
关键词 植物雌激素 染料木素 宫颈癌细胞 细胞周期 细胞 凋亡 雌激素受体ERα phytoestrogen genistein HeLa cells cellcycle cell apoptosis estrogen receptor ERα
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