天津医药

天津医药 ›› 2021, Vol. 49 ›› Issue (11): 1138-1142.doi: 10.11958/20210940

• 细胞与分子生物学 • 上一篇    下一篇

芹菜素对子宫内膜癌HEC-1-B细胞增殖和凋亡的影响及其机制研究

陈容，时艳华   

  1. 郑州澍青医学高等专科学校临床医学系（邮编450000）
  • 收稿日期:2021-04-19 修回日期:2021-07-19 出版日期:2021-11-15 发布日期:2021-11-19
  • 基金资助:
    河南省高等学校重点科研项目（17B320022）

The effect and its mechanism of apigenin on proliferation and apoptosis of HEC-1-B cells

CHEN Rong, SHI Yan-hua   

  1. Department of Clinical Medicine, Zhengzhou Shuqing Medical College, Zhengzhou 450000, China
  • Received:2021-04-19 Revised:2021-07-19 Published:2021-11-15 Online:2021-11-19

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摘要： 目的　研究芹菜素对子宫内膜癌细胞HEC-1-B增殖、侵袭、迁移、凋亡的影响及其作用机制。方法　取对数生长期的HEC-1-B细胞，加入0、20、40和80 μmol/L的芹菜素，采用CCK-8法检测培养24、48和72 h后细胞的光密度，计算增殖抑制率。流式细胞术检测细胞凋亡水平，Transwell实验检测细胞侵袭和迁移能力变化。Western blot检测凋亡相关蛋白Bax、Bcl-2以及磷脂酰肌醇3激酶（PI3K）、磷酸化PI3K（p-PI3K）、蛋白激酶B（AKT）和磷酸化AKT（p-AKT）的表达水平。结果　20~80 μmol/L范围内，随着芹菜素干预浓度的升高，HEC-1-B细胞的增殖明显受到抑制，细胞凋亡率升高，同时促凋亡蛋白Bax表达增高，抗凋亡蛋白Bcl-2表达下降。0、5、10和20 μmol/L范围内，随着芹菜素干预浓度的升高，HEC-1-B细胞侵袭和迁移能力下降。Western blot结果显示，40 μmol/L芹菜素能够下调PI3K/AKT通路蛋白p-PI3K和p-AKT的表达。结论　芹菜素能够抑制HEC-1-B细胞增殖、侵袭、迁移并促进其凋亡，其作用机制可能与PI3K/AKT信号通路有关。

关键词: 子宫内膜肿瘤, 芹菜素, 细胞增殖, 细胞凋亡, 细胞运动, PI3K/AKT信号通路

Abstract: Objective　To study the effect of apigenin on proliferation, invasion, migration and apoptosis of endometrial carcinoma cell line HEC-1-B cells and its mechanism. Methods　HEC-1-B cells in logarithmic growth phase were treated with 0, 20, 40 and 80 μmol/L apigenin. CCK-8 method was used to detect the absorbance of cells cultured for 24, 48 and 72 hours. The level of apoptosis was detected by flow cytometry, and the ability of invasion and migration were detected by Transwell assay. Western blot assay was used to detect the expression levels of Bax, Bcl-2, p-PI3K, PI3K, p-AKT and AKT. Results　With the increase of apigenin concentration from 20 to 80 μmol/L, the proliferation of HEC-1-B cells was significantly inhibited, the apoptosis rate increased. Meanwhile, the expression of pro-apoptotic protein Bax increased, and the expression of anti-apoptotic protein Bcl-2 decreased. With the increase of apigenin concentration in 0, 5, 10 and 20 μmol/L, the invasion and migration ability decreased in HEC-1-B cells. Western blot assay showed that 40 μmol/L apigenin could inhibit the expression levels of p-PI3K and p-AKT. Conclusion　Apigenin can inhibit the proliferation, invasion and migration, and promote apoptosis of HEC-1-B cells, which may be related to PI3K/AKT signaling pathway.

Key words: endometrial neoplasms, apigenin, cell proliferation, apoptosis, cell movement, PI3K/AKT signaling pathway