文章摘要
袁育珺.靛玉红诱导宫颈癌HeLa细胞凋亡及其机制的实验研究[J].安徽医药,待发表.
靛玉红诱导宫颈癌HeLa细胞凋亡及其机制的实验研究
投稿时间:2021-12-04  录用日期:2022-01-14
DOI:
中文关键词: 靛玉红  宫颈癌  凋亡  表达
英文关键词: 
基金项目:江西省卫生健康委基金(NO 202131091)
作者单位地址
袁育珺 九江学院附属医院 江西省九江市浔阳东路九江学院附属医院住院部二楼检验科
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中文摘要:
      摘要 目的 实验研究靛玉红对宫颈癌HeLa细胞的增殖、迁移和凋亡的影响及磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)信号通路在其中的作用。方法 选用人宫颈癌HeLa细胞株为细胞模型,随机分为正常对照组和靛玉红组。运用CCK-8、细胞划痕观察细胞的增殖和迁移状况;Hoechst33258染色、Annexin V-FITC分析细胞周期和凋亡的变化;免疫蛋白印迹分析凋亡及PI3K/AKT通路蛋白的表达变化。结果 与正常对照组比较,10、20、50 μmol/L靛玉红均抑制HeLa细胞的体外增殖和迁移,并呈时间和浓度依赖性(均P<0.05);Bcl-2、p-PI3K和p-AKT蛋白表达呈下降趋势,Bax、Caspase-3和Caspase-9表达呈上升趋势(均P<0.05)。Hoechst33258染色和Annexin V-FITC结果显示:10、20、50 μmol/L靛玉红能明显诱导HeLa细胞凋亡,且随浓度的升高中期凋亡和末期凋亡所占的比例明显上升。结论 靛玉红能抑制HeLa细胞体外增殖和迁移,并诱导其凋亡,其机制与下调PI3K/AKT信号通路相关。
英文摘要:
      Abstract Objective To study the effects of indirubin on the proliferation, migration and apoptosis of cervical cancer HeLa cells and the role of PI3K/AKT signaling pathway. Methods Human cervical cancer cell line HeLa was used as cell model and randomly divided into normal control group and indirubin group. Cell proliferation and migration were observed by CCK-8 and cell scratches. Cell cycle and apoptosis were analyzed by Hoechst33258 staining and Annexin V-FITC. Western blot analysis of apoptosis and protein expression of PI3K/AKT pathway. Results Compared with normal control group, 10, 20 and 50 μmol/L indirubin inhibited the proliferation and migration of HeLa cells in vitro in a time and concentration dependent manner (all P<0.05). The expressions of Bcl-2, p-PI3K and p-Akt showed a decreasing trend, while the expressions of Bax, Caspase-3 and Caspase-9 showed an increasing trend (all P<0.05). The results of Hoechst33258 staining and Annexin V-FITC showed that 10, 20 and 50 μmol/L indirubin could significantly induce apoptosis of HeLa cells, and the proportion of metaphase apoptosis and end-stage apoptosis increased with the increase of concentration. Conclution Indirubin can inhibit the proliferation and migration of HeLa cells in vitro and induce their apoptosis, and the mechanism is related to the down-regulation of PI3K/AKT signaling pathway.
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