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中医药调控程序性细胞死亡干预肝纤维化的研究进展

黄良江 毛德文 张荣臻 黄国初 王涵 秦伟彬 姚春

引用本文:
Citation:

中医药调控程序性细胞死亡干预肝纤维化的研究进展

DOI: 10.12449/JCH240127
基金项目: 

广西重点研发计划项目 (GK AB22035076)

广西研究生教育创新计划项目 (YCSW2022343)

广西学位与研究生教育改革课题“传承‘桂派名医名师’的中医硕士精英人才培养模式的探索与实践” (JGY2022182)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:毛德文、张荣臻负责对研究思路的设计;黄良江、王涵负责查阅相关文献,资料归纳、分析,撰写论文;秦伟彬、黄国初负责修改论文;姚春负责指导、审阅论文及最后定稿。
详细信息
    通信作者:

    姚春, yaochun111@163.com (ORCID: 0000-0003-2903-8814)

Research advances in traditional Chinese medicine regulation of programmed cell death in intervening against hepatic fibrosis

Research funding: 

Guangxi Key Research and Development Plan Projects (GK AB22035076);

Innovation Project of Guangxi Graduate Education (YCSW2022343);

Guangxi Degree and Graduate Education Reform Project “Exploration and Practice of the Training Mode of TCM Master Elite Talents by Inheriting ‘Guangxi Famous Doctors and Famous Teachers’” (JGY2022182)

More Information
  • 摘要: 肝纤维化(HF)是一种由于慢性肝损伤导致的肝组织结构异常修复的病理过程,其发病机制尚未完全阐明。相关研究表明,程序性细胞死亡可能与HF的发生有关,而中医药在调控程序性细胞死亡干预HF方面有着显著疗效。本文概述了程序性细胞死亡影响HF的主要机制,并从中医角度出发探讨中医药调控程序性细胞死亡改善HF的可能机制,为中医药防治肝纤维化提供新思路。

     

  • 表  1  近5年通过调控PCD抗肝纤维化的其他中药复方和中药活性成分总结

    Table  1.   Summary of other traditional Chinese medicine formulas and active ingredients for regulating PCD in the past five years to combat hepatic fibrosis

    类型 中药复方/中药有效成分 药物组成/有效成分来源 实验模型 作用机制及药理效应
    细胞凋亡 木脂素51 中药五味子主要提取物 CCl4诱导的HF小鼠模型 下调α-SMA/ETBR/PLCβ/CHOP/Bax、Caspase12/9/3凋亡因子表达,达到抗细胞凋亡和保肝作用
    桔梗皂苷D52 中药桔梗干燥根的提取物 体外HSC细胞模型 增加Bax、细胞色素C、cle-Caspase9/3凋亡蛋白的表达水平,减缓肝纤维化和HSC的活化
    杨桃根提取物53 杨桃根 CCl4诱导的HF大鼠模型 抑制α-SMA,TIMP2,TGF-β1,Smad2、3和4,BAX和Caspase3蛋白的表达,同时显著提高Smad7的mRNA表达以及Smad7和Bcl-2的蛋白表达,达到抗纤维化作用
    冬虫夏草菌丝体多糖、绞股蓝总皂苷和苦杏仁苷54 扶正化瘀胶囊主要成分 CCl4诱导的HF大鼠模型 降低ALT、AST水平,下调α-SMA、TGF-β1、Col-Ⅰ、Fas、TNF-R1、Caspase3/8/9/10、线粒体Bax、Bak和细胞色素C的蛋白表达
    黄芩素55 黄芩的主要活性成分 CCl4诱导的HF小鼠模型 增强HSC-T6细胞中cle-Caspase9/3表达和Bax/Bcl-2比例。通过调节HSC的活化和凋亡来减轻HF
    自噬 丹酚酸b56 丹参的根提取物 CCl4诱导的HF小鼠模型 抑制HSC激活的生物标志物(α-SMA和Ⅰ型胶原)表达,抑制HSC的活化和胶原沉积以减轻肝纤维化的发生
    益气柔肝汤57 太子参、生地、枸杞子、首乌、白术、白芍、茵陈、虎杖、苡仁、黄芪等 CCl4诱导的HF大鼠模型 下调MAPK和PI3K/Akt信号通路,上调PPAR和AMP活化蛋白激酶,改善肝功能、降低HSC活性和减少ECM沉积,以达到抗肝纤维化效果
    焦亡 合欢皮-白蒺藜药对58 中草药合欢皮、白蒺藜药对 体外细胞实验 下调NLRP3、caspase-1、α-SMA及GSDMD蛋白和基因表达,抑制细胞焦亡的经典通路,该机制可能参与其抗肝纤维化作用
    铁死亡 紫花前胡素59 白花前胡和紫花前胡根的提取物 CCl4诱导的HF小鼠模型 通过调节Gpx4和GSH水平下降,Fe2+、ROS和Ptgs2水平增加,以促进体外活化造血干细胞的铁死亡,达到HF作用
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  • 收稿日期:  2023-04-24
  • 录用日期:  2023-06-27
  • 出版日期:  2024-01-23
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