Article(id=1291339072816017976, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291339070622396983, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.03.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1715616000000, receivedDateStr=2024-05-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785808826876, onlineDateStr=2026-08-04, pubDate=1739721600000, pubDateStr=2025-02-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785808826876, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785808826876, creator=13041195026, updateTime=1785808826876, updator=13041195026, issue=Issue{id=1291339070622396983, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='3', pageStart='301', pageEnd='450', issueExtLink='null', onlineDate='null', pubDate='1739721600000', pubDateStr='2025-02-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785808826353, creator='13041195026', updateTime=1785897200933, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709740552310941, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291339070622396983, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709740552310942, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291339070622396983, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=335, endPage=339, ext={EN=ArticleExt(id=1291339073159950905, articleId=1291339072816017976, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=PX-478 ameliorates irradiation-induced apoptosis of cardiomyocytes, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the efficacy of the hypoxia-inducible factor-1α (HIF-1α) inhibitor PX-478 in improving radiation-induced apoptosis in cardiomyocytes and to elucidate its molecular mechanisms.
Methods H9c2 cells were divided into blank group, model group, experimental-L group and experimental-H group. The experimental-L, -H groups were cultured with PX-478 at concentrations of 5 and 10 mol·L-1, respectively, while the other groups were cultured in normal medium. After 24 h of culture, all groups except the blank group were irradiated with 6 Gy X-rays to establish a model of radiation-induced cardiac injury and were subsequently cultured for another 24 h. Cell viability was assessed using the cell counting kit-8 assay; relative protein expression levels were determined by Western blotting; and apoptosis was detected using Annexin V/PI flow cytometry.
Results The relative expression levels of HIF-1α protein in the blank group, model group, experimental-L group and experimental-H group were 0.89±0.01, 1.05±0.01, 0.64±0.02 and 0.52±0.02; the relative expression levels of aquaporin-1 (AQP1) protein were 0.79±0.02, 0.94±0.02, 0.74±0.01 and 0.59±0.01; AQP4 protein levels were 0.89±0.01, 1.03±0.01, 0.68±0.01 and 0.50±0.01; B-cell lymphoma-2 (Bcl-2) protein levels were 0.78±0.02, 0.58±0.02, 1.00±0.03 and 0.82±0.03; Bcl-2-associated X protein (Bax) levels were 0.66±0.01, 0.96±0.01, 0.77±0.01 and 0.27±0.03; Caspase-3 levels were 0.83±0.01, 1.10±0.01, 0.71±0.02 and 0.30±0.01; the apoptosis rates were (4.05±0.60)%, (17.82±0.63)%, (9.35±0.41)% and (9.07±0.57)%, respectively. The above indicators in the blank, experimental-L, experimental-H groups showed statistically significant differences compared to the model group (all P<0.05).
Conclusion PX-478 can improve radiation-induced cardiomyocyte edema and reduce apoptosis by inhibiting the abnormal activation of the HIF-1α/AQPs axis in H9c2 cells after irradiation, thereby regulating fluid metabolism.
, authors=Qi-yang LI
1, Shang-zu ZHANG
1, Yang-yang LI
1, Geng-qiang YANG
1, Li-ying ZHANG
1, 2, authorsList=Qi-yang LI, Shang-zu ZHANG, Yang-yang LI, Geng-qiang YANG, Li-ying ZHANG, authorCompany=null, correspAuthors=Li-ying ZHANG, 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=1291339073965257274, articleId=1291339072816017976, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=PX-478改善辐照诱导的心肌细胞凋亡的作用, 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 研究缺氧诱导因子-1 α（HIF-1α）抑制药（PX-478）改善辐射诱导的心肌细胞凋亡的有效性及其分子机制。
方法 将H9c2细胞分为空白组、模型组、低剂量实验组和高剂量实验组。低剂量实验组和高剂量实验组分别用5和10 mol·L-1的PX-478含药培养基培养，其他各组用正常培养基，培养24 h后，除空白组外，其余各组给予6 Gy X射线辐照建立放射性心脏损伤模型，继续培养24 h。用细胞计数-8法检测细胞活力，用蛋白质印迹法检测蛋白相对表达水平，用Annexin-V/PI流式凋亡检测法检测细胞的凋亡情况。
结果 空白组、模型组、低剂量实验组和高剂量实验组的HIF-1α蛋白相对表达水平分别为0.89±0.01、1.05±0.01、0.64±0.02和0.52±0.02，水通道蛋白1（AQP1）蛋白相对表达水平分别为0.79±0.02、0.94±0.02、0.74±0.01和0.59±0.01，AQP4蛋白相对表达水平分别为0.89±0.01、1.03±0.01、0.68±0.01和0.50±0.01，B淋巴细胞瘤-2（Bcl-2）蛋白相对表达水平分别为0.78±0.02、0.58±0.02、1.00±0.03和0.82±0.03，Bcl-2关联X蛋白（Bax）蛋白相对表达水平分别为0.66±0.01、0.96±0.01、0.77±0.01和0.27±0.03，胱天蛋白酶3（Caspase-3）蛋白相对表达水平分别为0.83±0.01、1.10±0.01、0.71±0.02和0.30±0.01，凋亡率分别为（4.05±0.60）%、（17.82±0.63）%、（9.35±0.41）%和（9.07±0.57）%。空白组、低剂量实验组和高剂量实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 PX-478可以通过抑制辐照后H9c2细胞HIF-1α/AQPs轴的异常激活，调节水液代谢，改善辐射诱导的心肌细胞水肿，减轻细胞凋亡。
, authors=李启杨
1, 张尚祖
1, 李洋洋
1, 杨更强
1, 张利英
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李启杨（1998-），男，博士研究生，主要从事中西医结合防治肿瘤的研究工作
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1.Key Laboratory for Molecular Medicine of Major Diseases and The Prevention and Treatment With Traditional Chinese Medicine Research in Gansu Colleges and Universities, Key Laboratory of Dunhuang Medicine and Transformation Ministry of Education, Gansu University of Traditional Chinese Medicine, Lanzhou 730000, Gansu Province, China
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