Article(id=1220655224029627029, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1220655218681893290, articleNumber=null, orderNo=null, doi=10.16438/j.0513-4870.2020-0444, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1585497600000, receivedDateStr=2020-03-30, revisedDate=1586620800000, revisedDateStr=2020-04-12, acceptedDate=null, acceptedDateStr=null, onlineDate=1768956484086, onlineDateStr=2026-01-21, pubDate=1589212800000, pubDateStr=2020-05-12, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1768956484086, onlineIssueDateStr=2026-01-21, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1768956484086, creator=13701087609, updateTime=1768956484086, updator=13701087609, issue=Issue{id=1220655218681893290, tenantId=1146029695717560320, journalId=1189982191388893191, year='2020', volume='55', issue='5', pageStart='773', pageEnd='1072', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1768956482811, creator=13701087609, updateTime=1768986431570, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1220780832940278305, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1220655218681893290, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1220780832940278306, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1220655218681893290, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=861, endPage=867, ext={EN=ArticleExt(id=1220655225048842948, articleId=1220655224029627029, tenantId=1146029695717560320, journalId=1189982191388893191, language=EN, title=Pirfenidone and nintedanib inhibit the lung alveolar regeneration in chronic pulmonary fibrosis mouse, columnId=1190335348761793317, journalTitle=Acta Pharmaceutica Sinica, columnName=Original Articles, runingTitle=null, highlight=null, articleAbstract=
The aim of this study was to determine whether the anti-fibrotic effects of pirfenidone (Pirf) and nintedanib (Nint) associated with the regulation of the alveolar epithelial type 2 cell (AEC II)-mediated lung alveolar regeneration in single- and multiple-dosage animal models of bleomycin-induced pulmonary fibrosis. All procedures involving animal treatment were approved according to the Committee on the Ethics of Animal Experiments of the Institute of Materia Medica, Chinese Academy of Medical Sciences. We found that the Pirf and Nint treatment of mice decreased the lung weight index, inflammation level, and the content of hydroxyproline compared with nontreated fibrotic mice in the single dosage model. Also, Pirf and Nint increased the oxygen saturation level and improved the lung functions in fibrotic mice, indicating that both drugs have anti-fibrotic effects in this model. However, the anti-fibrotic effects of Pirf and Nint were not observed in the multiple-dosage model. Further studies showed that Pirf and Nint decreased the expression of β-catenin, Axin2, c-Myc, Cyclin D1, and inhibited the Wnt/β-catenin signaling pathway, suggesting that Pirf and Nint did not produce anti-fibrotic effects in the multiple-dosage model due to their inhibiting the Wnt/β-catenin pathway and suppressing the stemness of AEC II, namely, suppressing AEC II-mediated lung alveolar regeneration.
, correspAuthors=Zhuo-wei HU, authorNote=null, correspAuthorsNote=null, copyrightStatement=Copyright ©2020 Acta Pharmaceutica Sinica. All rights reserved., 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, authorCompany=null, fund=null, authors=null, authorsList=Yun-xuan LI, Xiao-xi LÜ, Chang LIU, Shan-shan LIU, Zhuo-wei HU), CN=ArticleExt(id=1220655226600735501, articleId=1220655224029627029, tenantId=1146029695717560320, journalId=1189982191388893191, language=CN, title=吡非尼酮和尼达尼布抑制慢性肺纤维化小鼠肺泡上皮细胞再生, columnId=1190335348896011050, journalTitle=药学学报, columnName=研究论文, runingTitle=null, highlight=null, articleAbstract=
本研究探究了吡非尼酮（pirfenidone，Pirf）和尼达尼布（nintedanib，Nint）两种药物在单次及多次博莱霉素诱导的小鼠肺纤维化模型中，抗纤维化作用差异与肺泡II型上皮细胞（alveolar epithelial type 2 cell，AEC II）介导的肺泡再生之间的关系。本实验所有动物实验均通过中国医学科学院药物研究所伦理审查委员会审查。结果表明：在单次模型中，Pirf及Nint给药组小鼠的肺重指数显著降低，血氧饱和度显著回升，肺功能得到了明显改善，炎症评分显著降低，羟脯氨酸的含量显著下降，表明两种药物具有显著的抗纤维化作用；而在多次模型中两者均没有明显的抗纤维化作用。进一步研究表明Pirf和Nint能够降低β-catenin、Axin2、c-Myc和Cyclin D1蛋白的表达，抑制Wnt/β-catenin信号通路的活化，进而抑制AEC II的干性功能。以上结果提示，在多次模型中，Pirf和Nint两种药物没有明显的抗纤维化作用是由于药物抑制Wnt/β-catenin信号通路导致AEC II细胞的干性功能受阻，即AEC II细胞介导的肺泡再生受到了抑制。
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Pirfenidone (Pirf) or nintedanib (Nint) attenuates lung fibrosis in single dosage of bleomycin (sBLM) group. A: Schematic diagram of modeling and drug-delivering in the sBLM mice model. After 10 days of administration of a single dosage of bleomycin (3 U·kg<sup>-1</sup>), the mice were treated with Pirf (2 mg·kg<sup>-1</sup>) or Nint (1 mg·kg<sup>-1</sup>) for 10 days. Masson staining (B), lung index (C), SpO<sub>2</sub> level (D), lung function (E), inflammatory score, and hydroxyproline (F) were evaluated at 21 days after bleomycin-challenged. <sup>**</sup><i>P</i> < 0.01 <i>vs</i> sham group; <sup>△</sup><i>P</i> < 0.05, <sup>△△</sup><i>P</i> < 0.01 <i>vs</i> PBS-treated group. IC: Inspiratory capacity; Crs: Compliance of the respiratory system , figureFileSmall=+oRyWUDnywNxIWHzDhHlPg==, figureFileBig=KhYgD0h69uyjxtebLihHSA==, tableContent=null), ArticleFig(id=1220655230371414137, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=EN, label=null, caption=null, figureFileSmall=U6f/0dIE6yMXaOMrjHuUXg==, figureFileBig=WOZtMwQIRD9jhQlYDkFiFA==, tableContent=null), ArticleFig(id=1220655230493048967, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=CN, label=Figure 2, caption=
Pirf or Nint shows limited anti-fibrosis effects in multiple dosages of bleomycin (mBLM) group. A: Schematic diagram of modeling and drug-delivery in the mBLM mice model. Mice were intratracheally instilled bleomycin (1 U·kg<sup>-1</sup>) every two weeks for a total of 6 times. The mice were treated with Pirf (2 mg·kg<sup>-1</sup>) or Nint (1 mg·kg<sup>-1</sup>) 30 days after completing the last administration. Masson staining (B), lung index (C), SpO<sub>2</sub> level (D), lung function (E), inflammatory score, and hydroxyproline (F) were evaluated at 30 days after drug-delivering. <sup>**</sup><i>P</i> < 0.01 <i>vs</i> sham group , figureFileSmall=U6f/0dIE6yMXaOMrjHuUXg==, figureFileBig=WOZtMwQIRD9jhQlYDkFiFA==, tableContent=null), ArticleFig(id=1220655230614683796, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=EN, label=null, caption=null, figureFileSmall=ydHRzhOV7KiiwI6LoT4YGw==, figureFileBig=uRYbThoP1xTzQzA8W4P2DQ==, tableContent=null), ArticleFig(id=1220655230706958495, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=CN, label=Figure 3, caption=
Pirf or Nint inhibits the stemness of AEC II cell. Mouse AEC II cells were cultured in 50% Matrigel with fibroblasts, the exchange medium contained Pirf (1 mmol·L<sup>-1</sup>) or Nint (1 μmol·L<sup>-1</sup>), the cells were cultured for 30 days. Spheres images were collected with a microscope (A), and the colony area (B) and colony forming efficiency (C.F.E, C) were calculated. <sup>△△</sup><i>P</i> < 0.01 <i>vs</i> PBS group , figureFileSmall=ydHRzhOV7KiiwI6LoT4YGw==, figureFileBig=uRYbThoP1xTzQzA8W4P2DQ==, tableContent=null), ArticleFig(id=1220655230836981932, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=EN, label=null, caption=null, figureFileSmall=d9yEIZc7/WX0Dgyd3sTg3A==, figureFileBig=6Kfx+2cgm2ufEtyCgva9Ww==, tableContent=null), ArticleFig(id=1220655230933450936, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=CN, label=Figure 4, caption=
Pirf or Nint inhibits Wnt/<i>β</i>-catenin pathway. A549 cells were incubated with TGF-<i>β</i>1 (10 ng·mL<sup>-1</sup>), with or without Pirf (1 mmol·L<sup>-1</sup>) for 48 h. The expression of <i>β</i>-catenin, Axin2, c-Myc, and Cyclin D1 were analyzed with Western blotting (A, B). The relationship between Pirf treatment and Wnt/<i>β</i>-catenin pathway was evaluated with GSEA analysis (E). A549 cells were incubated with TGF-<i>β</i>1 (10 ng·mL<sup>-1</sup>), with or without Nint (1 μmol·L<sup>-1</sup>) for 48 h. The expression of <i>β</i>-catenin, Axin2, c-Myc, and Cyclin D1 were analyzed with Western blotting (C, D). The relationship between Nint treatment and Wnt/<i>β</i>-catenin pathway was evaluated with GSEA analysis (F) , figureFileSmall=d9yEIZc7/WX0Dgyd3sTg3A==, figureFileBig=6Kfx+2cgm2ufEtyCgva9Ww==, tableContent=null), ArticleFig(id=1220655231042502856, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=EN, label=null, caption=null, figureFileSmall=OzXpf75nkkcHJLnNwSxXuQ==, figureFileBig=4JH7bbmwJS8t/si8OKXYLw==, tableContent=null), ArticleFig(id=1220655231143166164, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1220655224029627029, language=CN, label=Figure 5, caption=
Schematic diagram of the difference between Pirf or Nint treatment in sBLM or mBLM animal model. After sBLM injury, the lung still has the ability to regenerate, but after mBLM injuries, the lung loses the ability to regenerate. Pirf or Nint not only has anti-fibrotic effects but also inhibits the lung regeneration ability , figureFileSmall=OzXpf75nkkcHJLnNwSxXuQ==, figureFileBig=4JH7bbmwJS8t/si8OKXYLw==, tableContent=null)], attaches=null, journal=Journal(id=1189982048455397383, delFlag=0, nameCn=药学学报, nameEn=Acta Pharmaceutica Sinica, nameHistory1=null, nameHistory2=null, issn=0513-4870, eissn=null, cn=11-2163/R, coden=null, periodic=0, language=CN, oaType=null, ccby=null, superviseOffice=null, ownerOffice=null, pubOffice=null, editorOffice=null, officeType=null, aims=null, clcCode=null, officeProv=null, officeCity=null, officeAddr=null, officeZip=null, officeEmail=null, officePhone=null, editDirector=null, officeDirector=null, officeDirectorPhone=null, officeStaffNum=null, officeEmpNum=null, coverPicUrl=BTxjudbJDVO4PqdBR6On6Q==, journalPrice=null, startedYear=null, abbrevIsoEn=null, journalRemark=null, publicationField=null, createdTime=1761643429151, updatedTime=1761735768113, createdBy=18614031015, 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