Article(id=1319291389171581716, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1319291312826863771, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.08.020, 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=1792473178427, onlineDateStr=2026-10-20, pubDate=1786291200000, pubDateStr=2026-08-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792473178427, onlineIssueDateStr=2026-10-20, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792473178427, creator=13701087609, updateTime=1792473178427, updator=13701087609, issue=Issue{id=1319291312826863771, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='8', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1786291200000', pubDateStr='2026-08-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792473160225, creator='13701087609', updateTime=1792473382588, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1319292245547799195, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1319291312826863771, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1319292245652656796, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1319291312826863771, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=91, endPage=96, ext={EN=ArticleExt(id=1319291389561651989, articleId=1319291389171581716, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Experimental Study of Celastrol Ameliorating Idiopathic Pulmonary Fibrosis by PTEN-mediated PI3K/PKB Signaling Pathway, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To observe the effect and mechanism of Celastrol extract on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling pathway mediated by phosphatase and tensin homolog (PTEN) in idiopathic pulmonary fibrosis (IPF) model mice.
Methods C57BL/6 mice were randomly divided into 4 groups with an average of 10 mice in each group, including normal group, model group, celastrol (1 mg·kg-1·d-1) group and pirfenidone (50 mg·kg-1·d-1) group. The IPF mouse model was established by intratracheal instillation of bleomycin (BLM). After successful modeling, each observation group was orally administered (ig), while the normal group was orally administered an equal amount of physiological saline for 28 consecutive days. The samples were taken out on the second day after the last administration. The pathological changes in lung tissue were observed through routine HE staining and collagen deposition in mouse lung interstitium and peribronchial tissue were observed through Masson special staining. Immunohistochemistry (IHC) method was used to detect the in situ expressions of PTEN and type I collagen in lung tissue, while quantitative real-time PCR (qRT-PCR)) was used to detect the mRNA expressions of PTEN, PI3K, PKB and interleukin (IL)-17β in lung tissue.
Results Compared with that of the normal group, the expression of type I collagen in the lung interstitium was significantly increased in the model group (P<0.05). The expressions of PI3K, PKB and IL-17β mRNA in lung tissue were significantly increased (P<0.05), and the expression of PTEN mRNA was significantly decreased (P<0.05). Compared with the model group, the celastrol and pirfenidone groups had a significant reduction in the expression of type I collagen in the lung tissue (P<0.05) and the expression of PTEN protein was significantly enhanced (P<0.05). The expressions of PI3K, PKB and IL-17β mRNA in lung tissue were significantly decreased (P<0.05), and the expression of PTEN mRNA was significantly increased (P<0.05).
Conclusion Celastrol extract can effectively inhibit the structural damage of lung interstitium and alleviate pulmonary fibrosis. The mechanism may be achieved by activating PTEN and coordinating the inhibition of PI3K/PKB expression, reducing inflammatory response and preventing the deposition of pulmonary interstitial collagen.
, authors=Honghong CHEN
1, Ke WU
1, Long LIN
1, Mingyue MO
1, Yulin ZHU
1, Yihuan LI
1, Yiping CHEN
1, Wanting LIU
1, Jiayan ZHANG
1, Yayi WU
1, Yuefeng FU
2, authorsList=Honghong CHEN, Ke WU, Long LIN, Mingyue MO, Yulin ZHU, Yihuan LI, Yiping CHEN, Wanting LIU, Jiayan ZHANG, Yayi WU, Yuefeng FU, authorCompany=null, correspAuthors=Yuefeng FU, 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=1319291390157243158, articleId=1319291389171581716, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=雷公藤红素对PTEN介导PI3K/PKB信号通路改善特发性肺纤维化的实验研究, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 观察雷公藤红素对磷酸酯酶与张力蛋白同源物(Phosphatase and tensin homolog,PTEN)介导磷脂酰肌醇3-激酶(Phosphatidyl inositol 3-kinase,PI3K)/蛋白激酶B(Protein kinase B,PKB)信号通路在特发性肺纤维化(Idiopathic pulmonary fibrosis,IPF)模型小鼠中的作用及机制。
方法 C57BL/6小鼠随机区组平均分为4组,每组10只,包括正常组、模型组、雷公藤红素(1 mg·kg-1·d-1)组、吡非尼酮组(50 mg·kg-1·d-1)。以气管滴注博来霉素(Bleomycin,BLM)的方法制备IPF小鼠模型。造模成功后,各观察组灌胃给药,正常组灌胃等量生理盐水,连续给药28 d,末次给药后第2天取材。HE常规病理染色观察肺组织病理变化,Masson特殊染色观察小鼠肺间质及支气管周围胶原沉积。免疫组化(Immunohistochemistry,IHC)检测PTEN以及I型胶原在肺组织中的原位表达,实时荧光定量PCR(Quantitative real-time PCR,qRT-PCR)检测肺组织中PTEN、PI3K、PKB及白细胞介素(interleukin,IL)-17βmRNA表达。
结果 与正常组相比,模型组肺间质I型胶原蛋白的表达显著增强(P<0.05),PTEN蛋白的表达明显减弱(P<0.05);肺组织匀浆PI3K、PKB及IL-17β mRNA表达均显著增强(P<0.05),PTEN mRNA表达显著减弱(P<0.05)。与模型组相比,雷公藤红素及吡非尼酮组肺间质I型胶原蛋白的表达明显减弱(P<0.05),PTEN蛋白的表达明显增强(P<0.05);肺组织匀浆PI3K、PKB及IL-17β mRNA表达显著减弱(P<0.05),PTEN mRNA表达显著增强(P<0.05)。
结论 雷公藤红素能有效抑制肺间质的结构破坏,减轻肺纤维化。其机制可能通过激活PTEN,并协调性抑制PI3K/PKB的表达,降低炎症反应,阻止肺间质胶原的沉积。
, authors=陈红红
1, 吴珂
1, 林龙
1, 莫名月
1, 朱裕林
1, 李熠桓
1, 陈依萍
1, 刘婉婷
1, 张嘉妍
1, 吴雅逸
1, 付跃峰
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陈红红(1989-),女,广东韶关人,讲师,硕士,研究方向:呼吸系统疾病机制。
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