Article(id=1208489301818590109, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1208489265789518263, articleNumber=null, orderNo=null, doi=10.16438/j.0513-4870.2021-0819, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1622563200000, receivedDateStr=2021-06-02, revisedDate=1625068800000, revisedDateStr=2021-07-01, acceptedDate=null, acceptedDateStr=null, onlineDate=1766055902199, onlineDateStr=2025-12-18, pubDate=1636646400000, pubDateStr=2021-11-12, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766055902199, onlineIssueDateStr=2025-12-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766055902199, creator=13701087609, updateTime=1766055902199, updator=13701087609, issue=Issue{id=1208489265789518263, tenantId=1146029695717560320, journalId=1189982191388893191, year='2021', volume='56', issue='11', pageStart='2881', pageEnd='3202', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1766055893609, creator=13701087609, updateTime=1766137012710, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1208829504026448153, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1208489265789518263, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1208829504026448154, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1208489265789518263, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=2950, endPage=2956, ext={EN=ArticleExt(id=1208489302439347169, articleId=1208489301818590109, tenantId=1146029695717560320, journalId=1189982191388893191, language=EN, title=Glaucocalyxin A represses TGF-β1-induced lung fibroblast differentiation by down-regulation of GSK3β/β-catenin signaling, columnId=1208489298932908784, journalTitle=Acta Pharmaceutica Sinica, columnName=Special Reports: Recent Advances in Visceral Organ Fibrosis and Antifibrotic Drug Discovery, runingTitle=null, highlight=null, articleAbstract=

In this study, we investigated the effect and mechanism of glaucocalyxin A on transforming growth factor-β1 (TGF-β1)-induced differentiation of lung fibroblasts by Western blotting, cellular immunofluorescence and collagen gel contraction assays. We monitored the phosphorylation of Smad3, measured extracellular regulated protein kinases (ERK) 1/2 and glycogen synthase kinse3β (Ser9) activity and the level of β-catenin to elucidate the role of glaucocalyxin A. The results show that glaucocalyxin A significantly decreased the expression of α-smooth muscle actin in lung fibroblasts; glaucocalyxin A remarkably reduced the formation of filaments and collagen gel contraction of lung fibroblasts; glaucocalyxin A notably down-regulated the production of fibronectin; glaucocalyxin A did not affect the phosphorylation level of Smad3 and ERK1/2; glaucocalyxin A markedly inhibited the phosphorylation of GSK3β (Ser9) and the levels of β-catenin; a GSK3β (S9A) mutant significantly inhibited lung fibroblast differentiation; and SKL2001, a β-catenin activator, partly reversed the inhibition of lung fibroblast differentiation by glaucocalyxin A. These results suggest that glaucocalyxin A significantly inhibits the differentiation of lung fibroblasts, which is related to the down-regulation of GSK3β/β-catenin signaling.

, correspAuthors=Xiao-gang JIANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=Copyright ©2021 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=Han-yue ZHU, Mei ZHU, Xi-hua CHEN, Xiao-gang JIANG), CN=ArticleExt(id=1208489306264551710, articleId=1208489301818590109, tenantId=1146029695717560320, journalId=1189982191388893191, language=CN, title=蓝萼甲素下调GSK3β/β-catenin信号通路抑制TGF-β1诱导的肺成纤维细胞转化, columnId=1208489300275086094, journalTitle=药学学报, columnName=专题报道：脏器纤维化疾病与抗纤维化药物研究, runingTitle=null, highlight=null, articleAbstract=

本研究探讨了蓝萼甲素抑制转化生长因子-β1（transforming growth factor-β1，TGF-β1）诱导的肺成纤维细胞向肺肌成纤维细胞转化的作用及其分子机制。应用Western blot法、细胞免疫荧光法、胶原胶收缩法等检测蓝萼甲素抑制TGF-β1诱导的肺成纤维细胞转化指标的变化情况；应用Western blot法、质粒转染法、激活剂等考察蓝萼甲素对TGF-β1诱导的肺成纤维细胞转化中Smad3、细胞外信号调节激酶（extracellular regulated protein kinases，ERK）、糖原合成酶激酶3β（glycogen synthase kinase 3β，GSK3β）（Ser9）三者的磷酸化水平与β-连环蛋白（β-catenin）表达情况及其调控作用。结果表明：蓝萼甲素能够显著降低肺成纤维细胞转化中α-平滑肌肌动蛋白（α-smooth muscle actin，α-SMA）表达水平；明显减少细胞肌丝的形成以及肺成纤维细胞胶原胶的收缩能力；显著下调纤维黏连蛋白（fibronectin，FN）的生成；不影响Smad3及ERK1/2的磷酸化水平；显著下调GSK3β（Ser9）的磷酸化及β-catenin的表达水平；GSK3β（S9A）突变体能明显抑制肺成纤维细胞转化；β-catenin激活剂SKL2001可部分逆转蓝萼甲素抑制肺成纤维细胞转化的作用。上述结果提示，蓝萼甲素能显著抑制肺成纤维细胞转化，这与蓝萼甲素下调GSK3β/β-catenin信号通路相关。

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