Article(id=1291338945216893014, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291338935477724120, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.01.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1719590400000, receivedDateStr=2024-06-29, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785808796258, onlineDateStr=2026-08-04, pubDate=1737043200000, pubDateStr=2025-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785808796258, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785808796257, creator=13041195026, updateTime=1785808796257, updator=13041195026, issue=Issue{id=1291338935477724120, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='1', pageStart='1', pageEnd='148', issueExtLink='null', onlineDate='null', pubDate='1737043200000', pubDateStr='2025-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785808794022, creator='13041195026', updateTime=1785808794022, updator='13041195026', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=45, endPage=49, ext={EN=ArticleExt(id=1291338946869448791, articleId=1291338945216893014, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of methyl oxofulnonone A ameliorates hyperglucose-induced H9c2 cardiomyocyte injury, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect and mechanism of methyl oxofulnonone A (META) on high glucose (HG)-induced H9c2 cell injury.
Methods H9c2 cells were divided into control group (normal culture), model group (55 mmol·L-1 glucose) and experimental -L, -M, -H groups (55 mmol·L-1 glucose+12.5, 25.0, 50.0 μmol·L-1 META). Cell viability was detected by cell counting kit-8; intracellular reactive oxygen species (ROS) level was detected by DCFH-DA fluorescent probe; intracellular adenosine triphosphate (ATP) content was detected by luciferase; and autophagy-related protein expression was detected by Western blotting.
Results The optical density values of 72-hour cells in the control group, model group and experimental -M, -H groups were 0.91±0.03, 0.61±0.01, 0.69±0.02 and 0.72±0.03; the ROS levels were (40.75±1.53)%, (43.73±1.30)%, (30.87±1.27)% and (28.28±1.43)%; the ATP contents were (8.16±0.71), (4.03±0.29), (5.29±0.31) and (5.83±0.31) nmol·mg-1; the relative expression levels of autophagy-related gene 5 protein were 1.05±0.06, 1.46±0.09, 0.98±0.11 and 0.89±0.09; the relative expression levels of ubiquitin-binding protein were 1.05±0.10, 0.55±0.13, 0.89±0.04 and 0.98±0.04; the ratios of microtubule-associated protein 1 light chain 3 Ⅱ/Ⅰ protein were 1.09±0.09, 1.82±0.05, 1.67±0.29 and 1.09±0.15, respectively. Among the above indicators, there were statistically significant differences between the model group and the control and experimental -M, -H groups (P<0.05, P<0.01).
Conclusion META significantly ameliorates H9c2 cardiomyocyte damage caused by high glucose, ameliorates oxidative stress, protects mitochondrial respiration and inhibits autophagy.
, authors=Ming-hui OUYANG
1, Xiao-tong GUO
1, Ting LIU
1, Li-ying CHENG
1, Zi-chang NIU
2, Hao-ping MAO
1, authorsList=Ming-hui OUYANG, Xiao-tong GUO, Ting LIU, Li-ying CHENG, Zi-chang NIU, Hao-ping MAO, authorCompany=null, correspAuthors=Hao-ping MAO, 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=1291338954389835865, articleId=1291338945216893014, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=甲基麦冬黄烷酮A改善高糖诱导H9c2心肌细胞损伤的作用研究, 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 研究甲基麦冬黄烷酮A（META）对高糖（HG）诱导H9c2细胞损伤的作用及机制。
方法 将H9c2细胞分为对照组（正常培养）、模型组（55 mmol·L-1葡萄糖）和低、中、高剂量实验组（55 mmol·L-1葡萄糖+12.5、25.0、50.0 μmol·L-1 META）。用细胞计数盒法-8法检测细胞活力，用DCFH-DA荧光探针检测细胞内活性氧（ROS）水平，用荧光素酶检测细胞内腺苷三磷酸（ATP）含量，用蛋白质印迹法检测自噬相关蛋白的表达水平。
结果 对照组、模型组和中、高剂量实验组的72 h细胞光密度值分别为0.91±0.03、0.61±0.01、0.69±0.02和0.72±0.03，ROS水平分别为（40.75±1.53）%、（43.73±1.30）%、（30.87±1.27）%和（28.28±1.43）%，ATP含量分别为（8.16±0.71）、（4.03±0.29）、（5.29±0.31）和（5.83±0.31）nmol·mg-1，自噬相关基因5蛋白相对表达水平分别为1.05±0.06、1.46±0.09、0.98±0.11和0.89±0.09，泛素结合蛋白P62蛋白相对表达水平分别为1.05±0.10、0.55±0.13、0.89±0.04和0.98±0.04，微管相关蛋白1轻链3Ⅱ/Ⅰ蛋白比值分别为1.09±0.09、1.82±0.05、1.67±0.29和1.09±0.15。中、高剂量实验组和对照组的上述指标与模型组相比，在统计学上差异均有统计学意义（P<0.05，P<0.01）。
结论 META显著改善高糖导致的H9c2心肌细胞损伤，改善氧化应激状态，保护线粒体呼吸功能和抑制细胞自噬。
, authors=欧阳明慧
1, 郭晓彤
1, 刘婷
1, 程丽颖
1, 牛子长
2, 毛浩萍
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欧阳明慧（1998-），女，硕士研究生，主要从事中药药理作用及药效物质的基础研究
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