Article(id=1292130449929827192, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130360968630762, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.06.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773849600000, receivedDateStr=2026-03-19, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997505885, onlineDateStr=2026-08-06, pubDate=1774627200000, pubDateStr=2026-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997505885, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997505885, creator=13701087609, updateTime=1785997505885, updator=13701087609, issue=Issue{id=1292130360968630762, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='6', pageStart='751', pageEnd='900', issueExtLink='null', onlineDate='null', pubDate='1774627200000', pubDateStr='2026-03-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997484675, creator='13701087609', updateTime=1786014452071, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201527440068743, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130360968630762, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201527440068744, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130360968630762, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=805, endPage=811, ext={EN=ArticleExt(id=1292130450173096825, articleId=1292130449929827192, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effect of ciprofibrate on pulmonary vascular remodeling in neonatal rats with hypoxic pulmonary hypertension by regulating the Ang2/Tie pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect of ciprofibrate on pulmonary vascular remodeling in neonatal rats with hypoxic pulmonary hypertension (HPH) by regulating the angiopoietin 2 (Ang2)/tyrosine protein kinase (Tie) pathway.
Methods Newborn rats were randomly separated into normal group, HPH group, low concentration ciprofibrate group, medium concentration ciprofibrate group, high concentration ciprofibrate group, and high concentration ciprofibrate + Ang2 activator rat Ang2 recombinant protein (rrAng2) group, with 12 rats in each group. Except for the normal group, newborn rats in all other groups were constructed with HPH models and administered once a day for 2 weeks starting from the first day of hypoxia. The changes in right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index were detected. Hematoxylin-eosin (HE) staining was applied to detect the pathology of lung tissue and the percentage of pulmonary artery middle layer wall thickness to its outer diameter (MT), and the percentage of pulmonary artery middle layer cross-sectional area to its total cross-sectional area (MA) changes. Immunofluorescence staining was applied to detect the relative fluorescence intensity of hypoxia inducible factor-1α (HIF-1α) and endothelin-1 (ET-1) in pulmonary arteries. Enzyme-linked immnosorbent assay (ELISA) was applied to detect levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-8 in pulmonary arteries. Western blot was applied to detect Ang2 and Tie2 proteins in pulmonary arteries.
Results Compared with the normal group, the HPH group showed an increase in pulmonary artery wall thickness and narrowing of the lumen, the RVSP, right ventricular hypertrophy index, MA, MT, HIF-1α, ET-1 relative fluorescence intensity, TNF-α, IL-8 levels, and Ang2 and Tie2 proteins in the pulmonary artery increased (P<0.05). Compared with the HPH group, the pulmonary artery wall thickening and luminal stenosis in rats in the low, medium, and high concentration ciprofibrate groups were improved, the RVSP, right ventricular hypertrophy index, MA, MT, HIF-1α, ET-1 relative fluorescence intensity, TNF-α, IL-8 levels, and Ang2 and Tie2 proteins in the pulmonary artery reduced (P<0.05). Compared with the high concentration ciprofibrate group, the high concentration ciprofibrate +rrAng2 group showed more significant thickening of the pulmonary artery wall and narrowing of the lumen in rats, the RVSP, right ventricular hypertrophy index, MA, MT, HIF-1α, ET-1 relative fluorescence intensity, TNF-α, IL-8 levels, and Ang2 and Tie2 proteins in the pulmonary artery increased (P<0.05).
Conclusion Ciprofibrate may improve pulmonary vascular remodeling in neonatal rats with HPH by inhibiting the Ang2/Tie pathway, thereby suppressing the expression of HIF-1α and ET-1 as well as the inflammatory response.
, authors=Li LIU
1, Rui-lin LI
2, Rong ZHU
1, Ming-mei ZHONG
3, authorsList=Li LIU, Rui-lin LI, Rong ZHU, Ming-mei ZHONG, authorCompany=null, correspAuthors=Ming-mei ZHONG, 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=1292130450613498746, articleId=1292130449929827192, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=环丙贝特调控Ang2/Tie通路对缺氧性肺动脉高压新生大鼠肺血管重塑的影响, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨环丙贝特调控血管生成素2（Ang2）/酪氨酸蛋白激酶（Tie）通路对缺氧性肺动脉高压（HPH）新生大鼠肺血管重塑的影响。
方法 新生大鼠随机分为正常组、HPH组、环丙贝特低浓度组、环丙贝特中浓度组、环丙贝特高浓度组、环丙贝特高浓度+Ang2激活剂大鼠Ang2重组蛋白（rrAng2）组，每组12只。除正常组外，其他组新生大鼠均需构建HPH模型，从缺氧第一天开始给药，每天给药1次，持续2周。检测右心室收缩压（RVSP）、右心室肥厚指数的变化；苏木精-伊红（HE）染色检测肺组织的病理及肺小动脉中层管壁厚度占其外径的百分比（MT）、肺小动脉中层横截面积占其总横截面积的百分比（MA）变化；免疫荧光染色检测肺动脉中缺氧诱导因子-1α（HIF-1α）、内皮素-1（ET-1）相对荧光强度；ELISA检测肺动脉中肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-8水平；Western blot检测肺动脉中Ang2、Tie2蛋白。
结果 与正常组相比，HPH组大鼠肺动脉壁厚增加，管腔狭窄，RVSP、右心室肥厚指数、MA、MT、肺动脉中HIF-1α、ET-1相对荧光强度、TNF-α、IL-8水平及Ang2、Tie2蛋白升高（P<0.05）；与HPH组相比，环丙贝特低、中、高浓度组大鼠肺动脉壁增厚及管腔狭窄现象有所改善，RVSP、右心室肥厚指数、MA、MT、肺动脉中HIF-1α、ET-1相对荧光强度、TNF-α、IL-8水平及Ang2、Tie2蛋白降低（P<0.05）；与环丙贝特高浓度组相比，环丙贝特高浓度+rrAng2组大鼠肺动脉壁增厚及管腔狭窄现象更明显，RVSP、右心室肥厚指数、MA、MT、肺动脉中HIF-1α、ET-1相对荧光强度、TNF-α、IL-8水平及Ang2、Tie2蛋白升高（P<0.05）。
结论 环丙贝特可能通过抑制Ang2/Tie通路抑制HIF-1α、ET-1表达及炎症反应进而改善HPH新生大鼠肺血管重塑。
, authors=刘莉
1, 李瑞麟
2, 朱蓉
1, 钟明媚
3, authorsList=刘莉, 李瑞麟, 朱蓉, 钟明媚, authorCompany=null, correspAuthors=钟明媚, authorNote=
刘莉（1980-），女，副主任医师，从事儿科内分泌、呼吸方面的研究
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