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中国应用生理学杂志 ›› 2019, Vol. 35 ›› Issue (3): 283-288.doi: 10.12047/j.cjap.5754.2019.059

• 研究论文 • 上一篇    

杨芽黄素对前列腺癌细胞凋亡的影响及其机制*

王瑜+, 柯瑞君, 蒋盼若+, 应佳豪+, 楼恩哲+, 陈佳玉   

  1. 绍兴文理学院医学院, 浙江 绍兴 312000
  • 出版日期:2019-05-28 发布日期:2019-06-28
  • 通讯作者: Tel: 0575-88345826; E-mail: chenyujia10@163.com. +: 为共同第一作者
  • 基金资助:
    国家自然科学基金资助项目(81402979);浙江省科技厅资助项目(2015C33270);浙江省卫生厅资助项目(2014KYA230); 国家级大学生创新训练项目(201810349028); 浙江省大学生科技创新活动计划项目(2018R432016); 绍兴市大学生创新项目(SXSDC201709)

The effects of tectochrysin on prostate cancer cells apoptosis and its mechanism

WANG Yu+, KE Rui-jun, JIANG Pan-ruo+, YING Jia-hao+, LOU En-zhe+, CHEN Jia-yu   

  1. Shaoxing University School of Medicine, Shaoxing 312000, China
  • Online:2019-05-28 Published:2019-06-28

摘要: 目的:探讨杨芽黄素对前列腺癌细胞22Rv.1的作用及机制。方法:将0~20 μg/ml杨芽黄素作用于22Rv.1细胞和正常前列腺细胞RWPE-1,适时采用MTS法检测细胞的增殖活性,采用流式细胞仪、hoechst染色、LDH释放实验分别检测22Rv.1细胞凋亡、死亡、周期、核型变化和药物的细胞毒作用,利用qPCR和Western blot分析22Rv.1细胞内基因转录和蛋白表达的改变,并通过抑瘤实验证实该药的抑癌作用。结果:杨芽黄素可显著抑制22Rv.1细胞增殖、诱导其凋亡,促进22Rv.1细胞凋亡相关基因dr4、dr5、trail、p53、caspase-3、caspase-8、caspase-9、bid、bax、foxo3的表达,并抑制抗凋亡基因akt、pi3k和bcl-2的表达。结论:杨芽黄素可通过影响TRAIL和PI3K/AKT信号通路诱导前列腺癌细胞凋亡,具有抗前列腺癌的作用。

关键词: 杨芽黄素, 前列腺癌细胞22Rv.1, TRAIL信号通路, PI3K/AKT信号通路, 细胞凋亡

Abstract: Objective: To investigate the effects of tectochrysin on prostate cancer cell line 22Rv.1 and reveal its molecular mechanism. Methods: Tectochrysin at the concentrations of 0~20 μg/ml was applied to 22Rv.1 cells and normal prostate cell RWPE-1. The proliferation activity of the cells was detected by MTS assay. Flow cytometry and hoechst 33342 staining were used to analyze the effects of drugs on cell apoptosis, death, cell cycle and nuclear type changes. LDH release test was used to analyze the cytotoxicity of the drug to 22Rv.1 cells. QPCR and Western blot were used to analyze the effects of the drug on the expressions of genes in 22Rv.1 cells. Finally, the tumor inhibited effect of the drug on the bearing tumor BALB/c mice were confirmed though anti-tumor experiment. Results: Tectochrysin could significantly inhibit the proliferation activity of 22Rv.1 cells and induced their apoptosis, and promoted the expressions of genes dr4, dr5, trail, p53, caspase-3, caspase-8, caspase-9, bid, bax and foxo3, inhibited the expressions of anti-apoptotic genes akt, pi3k and bcl-2. Conclusion: Tectochrysin can induce prostate cancer cells apoptosis through affecting TRAIL and PI3K/AKT signaling pathways, and has anti-prostate cancer effect.

Key words: tectochrysin, prostate cancer cell line 22Rv.1, TRAIL signal pathway, PI3K/AKT signal pathway, cell apoptosis

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