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木犀草素治疗肝损伤的作用机制

姜颖 高宁 王夏瑄 龚界 刘莉莉

引用本文:
Citation:

木犀草素治疗肝损伤的作用机制

DOI: 10.12449/JCH260231
基金项目: 

黑龙江中医药大学科研基金项目 (15041200003)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:姜颖负责课题设计,资料分析,撰写论文;高宁负责论文修改;王夏瑄、龚界参与收集数据;刘莉莉负责拟定写作思路,指导撰写文章并最后定稿。
详细信息
    通信作者:

    刘莉莉, liulili-liulili@163.com (ORCID: 0000-0003-4991-5984)

Mechanism of action of luteolin in treatment of liver injury

Research funding: 

Heilongjiang University of Traditional Chinese Medicine Scientific Research Fund Project (15041200003)

More Information
  • 摘要: 肝损伤已成为一项日益严峻的全球性健康难题,而现有化学药物存在疗效局限与不良反应等问题,亟需研发安全高效的新型治疗药物。近年研究发现,天然药用植物中的黄酮类化合物在肝损伤防治领域中展现出良好潜力。木犀草素作为典型天然黄酮成分,对多病因肝损伤均表现出良好的保护作用,但其作用机制尚未形成系统性阐释。本文归纳近年国内外相关研究进展,综述木犀草素在抑制氧化应激、抗炎、调控细胞死亡、抗肝纤维化、调节脂质代谢紊乱和调控肠-肝轴等方面的作用机制,并对其在肝损伤治疗中的应用前景进行展望,以期为该成分的深入研究提供科学参考。

     

  • 注: MDA,丙二醛;ROS,活性氧;HO-1,血红素加氧酶-1;SOD,超氧化物歧化酶;NQO1,醌氧化还原酶1;GSH,谷胱甘肽;Nrf2,核因子E2相关因子2;ARE,抗氧化反应元件;TLR,Toll样受体;IKK,κB抑制因子激酶;NF-κB,核因子κB;NLRP3,NOD样受体热蛋白结构域相关蛋白3;IL,白细胞介素;TNF-α,肿瘤坏死因子-α;iNo3,诱导型一氧化氮合酶;CD86,分化簇86;ARG-1,精氨酸酶1;CD206,分化簇206;ZO-1,紧密连接蛋白1;FD4,肝脂肪变程度;LPS,脂多糖;Bcl-2,B细胞淋巴瘤因子-2;Bax,Bcl-2相关X蛋白;Caspase,半胱氨酸天冬氨酸蛋白酶家族;mTOR,雷帕霉素靶蛋白;ACSL4,长链脂肪酸辅酶A合成酶4;ALOX15,花生四烯酸15-脂加氧酶;AMPK,腺苷酸活化蛋白激酶;GPX4,谷胱甘肽过氧化物酶4;ULK1,丝氨酸/苏氨酸特异性蛋白激酶;HP,羟脯氨酸;α-SMA,α-平滑肌肌动蛋白;TGF-β,转化生长因子-β;MMP-2,基质金属蛋白酶-2;TG,甘油三酯;Akt,3-激酶-蛋白激酶B;PI3K,磷脂酰肌醇-3-激酶;SREBP,甾醇调节元件结合蛋白。

    图  1  木犀草素对肝损伤的保护作用机制

    Figure  1.  Diagram of the protective mechanism of luteolin on liver injury

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