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中国精品科技期刊2020

6-姜烯酚抗肿瘤机制研究进展

王专 胡红柳 陈奇峰 周洁 任珍珍 蒋利和

王专,胡红柳,陈奇峰,等. 6-姜烯酚抗肿瘤机制研究进展[J]. 食品工业科技,2023,44(11):480−486. doi:  10.13386/j.issn1002-0306.2022080339
引用本文: 王专,胡红柳,陈奇峰,等. 6-姜烯酚抗肿瘤机制研究进展[J]. 食品工业科技,2023,44(11):480−486. doi:  10.13386/j.issn1002-0306.2022080339
WANG Zhuan, HU Hongliu, CHEN Qifeng, et al. Research Progress on Antitumor Mechanism of 6-Shogaol[J]. Science and Technology of Food Industry, 2023, 44(11): 480−486. (in Chinese with English abstract). doi:  10.13386/j.issn1002-0306.2022080339
Citation: WANG Zhuan, HU Hongliu, CHEN Qifeng, et al. Research Progress on Antitumor Mechanism of 6-Shogaol[J]. Science and Technology of Food Industry, 2023, 44(11): 480−486. (in Chinese with English abstract). doi:  10.13386/j.issn1002-0306.2022080339

6-姜烯酚抗肿瘤机制研究进展

doi: 10.13386/j.issn1002-0306.2022080339
基金项目: 南宁市青秀区重点研发项目(2020023);右江民族医学院高层次引进人才项目经费(YY2021sk02)。
详细信息
    作者简介:

    王专(1998−),男,硕士研究生,研究方向:食品营养学,E-mail:858812187@qq.com

    通讯作者:

    蒋利和(1976−),男,博士,研究员,研究方向:肿瘤药理学、食品营养学,E-mail:jianglihe@gxu.edu.cn

  • 中图分类号: R15

Research Progress on Antitumor Mechanism of 6-Shogaol

  • 摘要: 癌症的发病率与死亡率逐年递增,严重威胁人类健康。6-姜烯酚是生姜中一种主要活性成分,因其具有安全、低毒的优势成为国内外学者关注的热点,6-姜烯酚具有抗炎、抗氧化、抗肿瘤等药理作用,尤其是其抗肿瘤活性日趋成为研究焦点。本文对6-姜烯酚的抗肿瘤作用机制进行综述,主要包括抑制细胞增殖、诱导细胞凋亡、阻滞细胞周期、抑制细胞的迁移和侵袭、影响肿瘤细胞自噬等,以期为6-姜烯酚抗肿瘤的进一步研究、开发和应用提供思路。
  • 图  1  6-姜烯酚的化学结构

    Figure  1.  Chemical structure of 6-shogaol

    图  2  6-姜烯酚在肿瘤细胞中的促凋亡机制

    Figure  2.  Proapoptotic mechanism of 6-shogaol in tumor cells

    图  3  6-姜烯酚在肿瘤细胞中抑制增殖的作用机制

    Figure  3.  Mechanism of 6-shogaol inhibiting proliferation in tumor cells

    图  4  6-姜烯酚在肿瘤细胞中抑制迁移和侵袭的作用机制

    Figure  4.  Mechanism of 6-shogaol in inhibiting migration and invasion of tumor cells

    图  5  6-姜烯酚在肿瘤细胞中影响自噬的作用机制

    Figure  5.  Mechanism of 6-shogaol affecting autophagy in tumor cells

    表  1  6-姜烯酚的抗肿瘤作用及其机制

    Table  1.   Antitumor effect and its mechanism of 6-shogaol

    药理作用癌症类型癌症细胞系或动物模型作用机制参考文献
    抑制肿瘤细胞增殖肝癌Bel-7402调控Wnt/β-Catenin信号通路[7]
    HepG2Bax、细胞色素C和Caspase3表达升高[28]
    乳腺癌MCF-7和T47D靶向Notch信号通路,抑制细胞自噬[8]
    口腔癌YD-10B和Ca9-22调控PI3K/AKT/mTOR信号通路[10]
    OC2显著增加Ca2+含量,影响内质网功能[63]
    8~10周龄的雄性金色叙利亚仓鼠NF-κB和AP-1致癌信号来减轻炎症和细胞增殖[64]
    胰腺癌Panc-1、AsPC-1、BxPC-3、CAPAN-2、CFPAC-1、MIAPaCa-2和SW1990通过影响内源性线粒体功能,造成Caspase3释放[12]
    结肠癌COLO 205ROS水平升高,Bax、Fas、FasL表达上调,Bcl-2、Bcl-XL表达下调[36]
    脂肪肉瘤SW872和93T449调控STAT-3、AMPK信号通路,影响内质网功能[21]
    诱导肿瘤细胞凋亡肝癌Bel-7402、HepG2调控Wnt/β-Catenin信号通路[7]
    SMMC-7721抑制elF-2α的磷酸化,影响内质网应激[39]
    前列腺癌LNCaP、DU145和PC3调控STAT3和 NF-κB信号通路[16]
    结肠癌HCT-116、SW-480和HT-29促进Bax、Caspase3和PARP1蛋白的表达,抑制Bcl-2的表达[24, 26]
    胃癌BGC-823调控EMT信号通路[29]
    淋巴癌CCRF-CEM和Nalm-6调控p53信号通路,影响ROS水平[32]
    宫颈癌HeLa和SiHa通过影响线粒体功能,进而影响ROS,
    造成Caspase3释放
    [27, 54]
    阻滞肿瘤细胞周期前列腺癌LNCaP、DU145和PC3p21和p27蛋白表达明显升高,Cyclin D1蛋白表达下降[16]
    肺癌H1650、H520和H1975下调Cyclin D1和Cyclin D3,调控Akt[47]
    宫颈癌HeLa显著下调Cyclin B1、PCNA表达,上调p21蛋白表达[27]
    结肠癌HCT-116和SW480上调p53蛋白和CDK抑制剂表达,下调cdc2蛋白表达[46]
    淋巴癌CCRF-CEM和Nalm-6调控p53信号通路,影响ROS水平[32]
    抑制肿瘤细胞迁移和侵袭肝癌Hep3B调控NF-κB、MAPK信号通路[51]
    乳腺癌MDA-MB231调控Hedgehog/Gli1通路[52]
    胃癌BGC-823调控EMT信号通路[29]
    口腔癌YD-10B和Ca9-22调控Akt信号通路[10]
    宫颈癌HeLa与ECM信号通路相关蛋白表达水平有关[54]
    影响肿瘤细胞自噬肺癌A549阻断Akt-mTOR信号通路,诱导细胞自噬[65]
    肝癌Huh7通过影响p53和ROS水平,导致自噬通量衰减[59]
    乳腺癌MCF-7抑制beclin-ILC3-II的表达,抑制细胞自噬[8]
    结肠癌HT29形成大量自噬小体,Caspase3和Caspase7活性升高[57]
    下载: 导出CSV
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出版历程
  • 收稿日期:  2022-08-31
  • 网络出版日期:  2023-04-18
  • 刊出日期:  2023-06-01

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