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中国应用生理学杂志 ›› 2022, Vol. 38 ›› Issue (5): 520-524.doi: 10.12047/j.cjap.6259.2022.097

• 研究论文 • 上一篇    下一篇

紫云英苷对未分化胃癌细胞凋亡的影响 *

褚智恒+, 何施燕+, 王瑜, 朱若婷, 顾益玲, 陈佳玉   

  1. 绍兴文理学院医学院, 浙江 绍兴 312000
  • 收稿日期:2022-01-20 修回日期:2022-09-28 出版日期:2022-09-28 发布日期:2023-04-23
  • 通讯作者: Tel: 0575-88345826; E-mail: chenyujia10@163.com
  • 作者简介:+: 为共同第一作者
  • 基金资助:
    *国家级大学生创新创业训练计划项目(202010349038)

Effects of Astragalin on apoptosis of undifferentiated gastric cancer cells

CHU Zhi-heng+, HE Shi-yan+, WANG Yu, ZHU Ruo-ting, GU Yi-ling, CHEN Jia-yu   

  1. Shaoxing University School of Medicine, Shaoxing 312000, China
  • Received:2022-01-20 Revised:2022-09-28 Online:2022-09-28 Published:2023-04-23

摘要: 目的: 探讨紫云英苷(Astragalin)对未分化胃癌细胞HGC-27的作用及相关分子机制。方法: 将紫云英苷作用HGC-27细胞,设置对照组(0 μg/ml)和Astragalin组(12.5、25、50 μg/ml),每组设置3复孔,用CCK-8法分别在用药0、24、48、72 h后检测细胞增殖活性; 在浓度为0、50 μg/ml的Astragalin作用24 h后,倒置显微镜下观察细胞形态,hoechst 33342、JC-1染色观察其核形和线粒体膜电位,流式细胞仪检测细胞周期和凋亡率的改变,二代测序仪分析基因的逆转录水平。结果: 紫云英苷可明显抑制HGC-27的增殖(P<0.01),下调细胞线粒体膜电位,诱导细胞凋亡,使细胞周期阻滞于G1期(P<0.01)。同时,紫云英苷上调基因bax、bad的转录水平,抑制egf、egfr、pik3cb、pdk1、akt3、bcl-2和sgk3基因的转录(P<0.01)。Western blot实验也证实紫云英苷降低PI3K和AKT蛋白的表达,同时BAX和BCL-2蛋白的比例也显著增加(P<0.01)。结论: 紫云英苷可通过抑制EGFR/PDK/AKT信号通路诱导未分化型胃癌细胞HGC-27凋亡,并将细胞周期阻滞于G1期,对未分化胃癌具有一定的治疗作用。

关键词: 紫云英苷, 胃癌, 信号通路, 细胞凋亡, 细胞培养

Abstract: Objective: To investigate the effects and related molecular mechanisms of Astragalin on undifferentiated gastric cancer cell HGC-27. Methods: Astragalin was used to treat HGC-27 cells, the cell proliferation activity was detected by CCK-8 method, the cell morphology was observed under inverted microscope, hoechst 33342 and JC-1 staining were used to observe the changes of nucleus formation and mitochondrial membrane potential, the cell cycle and apoptosis rate were detected by flow cytometry, the reverse transcription level of the gene was analyzed by the second-generation sequencer. Results: Astragalin inhibited the proliferation of HGC-27 significantly (P<0.01), down-regulated mitochondrial membrane potential, induced cell apoptosis, blocked the cell cycle in G1 prophase. At the same time, Astragalin up-regulated the transcription levels of genes bax and bad, down-regulated the transcription levels of genes egf, egfr, pik3cb, pdk1, akt3 and bcl-2. Western blot analysis also showed that the expressions of PI3K and Akt protein were decreased, and the proportion of Bax and BCL-2 protein was increased significantly (P<0.01). Conclusion: The apoptosis of undifferentiated gastric cancer cell line HGC-27 can be induced by Astragalin through inhibition of EGFR/PDK/Akt signaling pathway, and the cell cycle can be blocked in G1 phase, which has a certain therapeutic effect on undifferentiated gastric cancer.

Key words: Astragalin, gastric cance, signaling pathway, cell apoptosis, cell culture

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