Article(id=1322928277354054591, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.10.021, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793340280140, onlineDateStr=2026-10-30, pubDate=1760025600000, pubDateStr=2025-10-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793340280140, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793340280140, creator=13701087609, updateTime=1793340280140, updator=13701087609, issue=Issue{id=1322926740955341011, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='10', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1760025600000', pubDateStr='2025-10-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793339913834, creator='13701087609', updateTime=1793340753123, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322930261259846420, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322930261259846421, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322926740955341011, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=102, endPage=107, ext={EN=ArticleExt(id=1322928277555381184, articleId=1322928277354054591, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Research Progress of Mechanism of Danggui Buxue Decoction(当归补血汤)in Organ Fibrosis, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Organ fibrosis is considered as a kind of tumor lesion with complex mechanism and difficult prevention and treatment,which is the focus and difficulty of medical research.Due to its multi-target and multi-mechanism characteristics,traditional Chinese medicine has been widely concerned in organ fibrosis,especially the role of invigorating Qi and activating blood.Danggui Buxue Decoction(当归补血汤,DBD),composed of Huangqi(Astragali Radix)and Danggui(Angelicae Sinensis Radix),is a representative prescription of invigorating Qi and activating blood,and has shown therapeutic effects in a variety of organ fibrosis.Therefore,this paper summarized the research progress of DBD in organ fibrosis of lung,kidney,liver and heart in recent 20 years.It is found that the mechanism of action of DBD against organ fibrosis is related to the regulation of TGF-β1/Smad signaling pathway,the improvement of extracellular matrix deposition,the regulation of neovascularization,anti-oxidative stress,anti-inflammation and the regulation of apoptosis.It provides a reference for the clinical application and mechanism study of DBD in organ fibrosis.
, authors=Yuwei ZHANG, Ganggang LI, Yanwei HAO, Wenjia XIAN, Yutong ZOU, Fei WANG, Quanyu DU, authorsList=Yuwei ZHANG, Ganggang LI, Yanwei HAO, Wenjia XIAN, Yutong ZOU, Fei WANG, Quanyu DU, authorCompany=null, correspAuthors=Fei WANG, Quanyu DU, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1322928278209692609, articleId=1322928277354054591, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=当归补血汤在器官纤维化中的作用机制进展, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
器官纤维化被认为是一种类肿瘤病变,其机制复杂,防治困难,是医学研究的重点与难点。中医药因其多靶点、多机制的特点,在器官纤维化中受到广泛关注,其中尤以益气活血类中药的作用最为突出。由黄芪、当归配伍组成的当归补血汤,是益气活血法的代表性方剂,在多种器官纤维化中都表现出治疗作用。因此,总结了最近20年当归补血汤在肺、肾、肝、心等器官纤维化中的研究进展。发现当归补血汤抗器官纤维化的作用机制与调控TGF-β1/Smad信号通路、改善细胞外基质沉积、调节血管新生、抗氧化应激、抗炎、调控细胞凋亡等相关。为当归补血汤在器官纤维化的临床应用和机制研究提供参考。
, authors=张雨薇, 李刚刚, 郝彦伟, 鲜文佳, 邹雨彤, 王飞, 杜全宇, authorsList=张雨薇, 李刚刚, 郝彦伟, 鲜文佳, 邹雨彤, 王飞, 杜全宇, authorCompany=null, correspAuthors=王飞, 杜全宇, authorNote=
张雨薇(1992-),女,四川宜宾人,主治医师,硕士,研究方向:中医药防治呼吸病的临床与基础。
, correspAuthorsNote=
杜全宇(1983-),女,重庆人,副教授,硕士研究生导师,硕士,研究方向:中医药防治呼吸病的临床与基础。E-mail:
quanydu@163.com。
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张雨薇(1992-),女,四川宜宾人,主治医师,硕士,研究方向:中医药防治呼吸病的临床与基础。
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张雨薇(1992-),女,四川宜宾人,主治医师,硕士,研究方向:中医药防治呼吸病的临床与基础。
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| 器官 | 模型 | 干预物 | 作用及机制 | 参考文献 |
|---|
| 肺脏 | BLM诱导的PF大鼠 | DBDG/DBD | 血清HA、LN、PCⅢ、COL-Ⅳ、MMP-9、TIMP-1 mRNA下降,平衡MMP/TIMP系统 | [12-13, 20-21, 23, 25, 29-30, 32] |
| | | MDA、NADPH氧化酶4下降,GSH-Px、SOD上升,改善脂质过氧化 | |
| 肺指数、炎症评分、Ashcroft评分、胶原体积分数、HYP、α-SMA、COL-I、COL-Ⅲ、TNF-α、IL-6、IL-1 β、TGF-β1、Smad3、纤溶酶原激活物抑制因子-1下降 |
| | | HIF-1 α、血小板源生长因子下降,色素上皮衍生因子、重组人血管内皮抑制素上升 | |
| | | NLRP3、Toll样受体4、髓样分化因子88、NF-κB、凋亡相关斑点样蛋白和含半胱氨酸的天冬氨酸蛋白水解酶1下降 | |
| | | B淋巴细胞瘤-2相关X蛋白、PI3K、AKT、mTOR下降,B淋巴细胞瘤-2上升 | |
| TGF-β1诱导的HLF-1细胞 | DBDG | HYP、α-SMA、COL-Ⅰ、COL-ⅢmRNA下降,MMP-9上升,抑制细胞增殖 | [11] |
| 平阳霉素诱导的PF大鼠 | DBDG | MDA、TGF-β1、HYP下降,GSH-Px、SOD上升 | [16] |
| BLM诱导的PF大鼠、TGF-β1诱导MRC-5细胞 | 黄芪甲苷、阿魏酸 | Smad泛素化调节因子2下降,Smad7、Smad核转录共抑制因子上升,抑制细胞增殖,调控TGF-β1/Smad通路 | [10, 17] |
| TGF-β1诱导的肌成纤维细胞 | 槲皮素和山柰酚 | 肌成纤维细胞活化下降 | [9] |
| IPF患者 | DBD联合泼尼松 | 炎性因子下降,改善患者的中医证候,提高运动耐力和生命质量 | [26] |
| BLM诱导的PF小鼠 | 黄芪当归药对 | VEGF mRNA下降,c-kit原癌基因,碱性成纤维细胞生长因子2 mRNA上升 | [19, 27] |
| | | TGF-β、IL-6、维甲酸相关孤儿受体γt mRNA下降 | |
| 肾脏 | 腺嘌呤诱导的RF大鼠 | DBD水、醇提取物 | 骨形态发生蛋白-7及mRNA上升,TGF-β1蛋白及mRNA降低 | [35] |
| 高脂饮食诱发的糖尿病肾病GK大鼠 | DBD | IL-6、IL-10、TNF-α、TGF-β1、Smad3、COL-Ⅳ、α-SMA、C-反应蛋白和波形蛋白下降,Smad5上升,调控TGF-β1/Smad信号通路 | [36] |
| UUO大鼠 | 黄芪甲苷Ⅳ和阿魏酸 | 肾小管上皮间质转化和成纤维细胞活化减少 | [37] |
| | DBD | NLRP3、IL-1 β、肾间质纤维化评分降低 | [43] |
| | 归芪口服液 | TGF-β1、α-SMA、血管紧张素Ⅱ减少 | [45] |
| 高糖诱导的GMC | DBD | FN、LN、COL-Ⅳ下降,细胞增殖减少 | [41, 64-65] |
| 高糖诱导的HK-2 | DBD | COL-Ⅳ、α-SMA、TGF-β1、波形蛋白、miR-27a降低,细胞增殖减少,调控miR-27a/TGF-β1/Smad3信号通路 | [42] |
| DN气虚血瘀证患者 | DBD | 空腹血糖、糖化血红蛋白、24 h尿蛋白、血尿素氮、尿蛋白、COL-Ⅳ、LN下降 | [39] |
| 肝脏 | CCL 4致HF大鼠、小鼠 | DBD | MDA、MMP-2/9、HIF-1α下降,SOD上升,调节脂质过氧化,改善肝功能VEGF、血管生成素1下降,抑制肝血管新生 | [53-54] |
| | | IL-6、TNF-α、IL-1 β、PI3K、AKT、c-Jun、JNK、p38 MAPK下降 | [50] |
| LX-2细胞,二甲基亚硝胺诱导的HF小鼠 | 黄芪甲苷Ⅰ、欧当归内酯A、毛蕊异黄酮 | α-SMA、COL-Ⅰ、HYP降低 | [51] |
| 血吸虫病HF家兔 | DBD | 血清HYP及HA下降,B超声像、组织病理学改善 | [52, 66] |
| 心脏 | 异丙肾上腺素诱导MF大鼠 | DBD | HYP降低,左心功能改善 | [58] |
| 心肌梗死后MF小鼠 | DBD | 心肌胶原容积分数降低,心室重塑减少 | [59] |
| 经腹主动脉不完全结扎诱发的MF大鼠 | DBD | COL-Ⅰ、COL-Ⅲ、COL-Ⅳ减少,抑制肾素-血管紧张素-醛固酮系统活性 | [60] |
| 尿毒症MF大鼠 | DBD | TGF-β1、瞬时受体电位M7降低 | [61] |
| 其他 | 腹膜透析的大鼠 | DBD | 间皮细胞脱落、成纤维细胞、炎症细胞、血管增生减少,腹膜增厚程度减轻 | [62] |
), ArticleFig(id=1322928283356103668, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322928277354054591, language=CN, label=表1, caption=
当归补血汤的抗纤维化作用及机制
, figureFileSmall=null, figureFileBig=null, tableContent=
| 器官 | 模型 | 干预物 | 作用及机制 | 参考文献 |
|---|
| 肺脏 | BLM诱导的PF大鼠 | DBDG/DBD | 血清HA、LN、PCⅢ、COL-Ⅳ、MMP-9、TIMP-1 mRNA下降,平衡MMP/TIMP系统 | [12-13, 20-21, 23, 25, 29-30, 32] |
| | | MDA、NADPH氧化酶4下降,GSH-Px、SOD上升,改善脂质过氧化 | |
| 肺指数、炎症评分、Ashcroft评分、胶原体积分数、HYP、α-SMA、COL-I、COL-Ⅲ、TNF-α、IL-6、IL-1 β、TGF-β1、Smad3、纤溶酶原激活物抑制因子-1下降 |
| | | HIF-1 α、血小板源生长因子下降,色素上皮衍生因子、重组人血管内皮抑制素上升 | |
| | | NLRP3、Toll样受体4、髓样分化因子88、NF-κB、凋亡相关斑点样蛋白和含半胱氨酸的天冬氨酸蛋白水解酶1下降 | |
| | | B淋巴细胞瘤-2相关X蛋白、PI3K、AKT、mTOR下降,B淋巴细胞瘤-2上升 | |
| TGF-β1诱导的HLF-1细胞 | DBDG | HYP、α-SMA、COL-Ⅰ、COL-ⅢmRNA下降,MMP-9上升,抑制细胞增殖 | [11] |
| 平阳霉素诱导的PF大鼠 | DBDG | MDA、TGF-β1、HYP下降,GSH-Px、SOD上升 | [16] |
| BLM诱导的PF大鼠、TGF-β1诱导MRC-5细胞 | 黄芪甲苷、阿魏酸 | Smad泛素化调节因子2下降,Smad7、Smad核转录共抑制因子上升,抑制细胞增殖,调控TGF-β1/Smad通路 | [10, 17] |
| TGF-β1诱导的肌成纤维细胞 | 槲皮素和山柰酚 | 肌成纤维细胞活化下降 | [9] |
| IPF患者 | DBD联合泼尼松 | 炎性因子下降,改善患者的中医证候,提高运动耐力和生命质量 | [26] |
| BLM诱导的PF小鼠 | 黄芪当归药对 | VEGF mRNA下降,c-kit原癌基因,碱性成纤维细胞生长因子2 mRNA上升 | [19, 27] |
| | | TGF-β、IL-6、维甲酸相关孤儿受体γt mRNA下降 | |
| 肾脏 | 腺嘌呤诱导的RF大鼠 | DBD水、醇提取物 | 骨形态发生蛋白-7及mRNA上升,TGF-β1蛋白及mRNA降低 | [35] |
| 高脂饮食诱发的糖尿病肾病GK大鼠 | DBD | IL-6、IL-10、TNF-α、TGF-β1、Smad3、COL-Ⅳ、α-SMA、C-反应蛋白和波形蛋白下降,Smad5上升,调控TGF-β1/Smad信号通路 | [36] |
| UUO大鼠 | 黄芪甲苷Ⅳ和阿魏酸 | 肾小管上皮间质转化和成纤维细胞活化减少 | [37] |
| | DBD | NLRP3、IL-1 β、肾间质纤维化评分降低 | [43] |
| | 归芪口服液 | TGF-β1、α-SMA、血管紧张素Ⅱ减少 | [45] |
| 高糖诱导的GMC | DBD | FN、LN、COL-Ⅳ下降,细胞增殖减少 | [41, 64-65] |
| 高糖诱导的HK-2 | DBD | COL-Ⅳ、α-SMA、TGF-β1、波形蛋白、miR-27a降低,细胞增殖减少,调控miR-27a/TGF-β1/Smad3信号通路 | [42] |
| DN气虚血瘀证患者 | DBD | 空腹血糖、糖化血红蛋白、24 h尿蛋白、血尿素氮、尿蛋白、COL-Ⅳ、LN下降 | [39] |
| 肝脏 | CCL 4致HF大鼠、小鼠 | DBD | MDA、MMP-2/9、HIF-1α下降,SOD上升,调节脂质过氧化,改善肝功能VEGF、血管生成素1下降,抑制肝血管新生 | [53-54] |
| | | IL-6、TNF-α、IL-1 β、PI3K、AKT、c-Jun、JNK、p38 MAPK下降 | [50] |
| LX-2细胞,二甲基亚硝胺诱导的HF小鼠 | 黄芪甲苷Ⅰ、欧当归内酯A、毛蕊异黄酮 | α-SMA、COL-Ⅰ、HYP降低 | [51] |
| 血吸虫病HF家兔 | DBD | 血清HYP及HA下降,B超声像、组织病理学改善 | [52, 66] |
| 心脏 | 异丙肾上腺素诱导MF大鼠 | DBD | HYP降低,左心功能改善 | [58] |
| 心肌梗死后MF小鼠 | DBD | 心肌胶原容积分数降低,心室重塑减少 | [59] |
| 经腹主动脉不完全结扎诱发的MF大鼠 | DBD | COL-Ⅰ、COL-Ⅲ、COL-Ⅳ减少,抑制肾素-血管紧张素-醛固酮系统活性 | [60] |
| 尿毒症MF大鼠 | DBD | TGF-β1、瞬时受体电位M7降低 | [61] |
| 其他 | 腹膜透析的大鼠 | DBD | 间皮细胞脱落、成纤维细胞、炎症细胞、血管增生减少,腹膜增厚程度减轻 | [62] |
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