Article(id=1291404690055487852, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404681641713991, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.07.007, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1729353600000, receivedDateStr=2024-10-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824471248, onlineDateStr=2026-08-04, pubDate=1744819200000, pubDateStr=2025-04-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824471248, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824471248, creator=13701087609, updateTime=1785824471248, updator=13701087609, issue=Issue{id=1291404681641713991, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='7', pageStart='901', pageEnd='1050', issueExtLink='null', onlineDate='null', pubDate='1744819200000', pubDateStr='2025-04-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824469242, creator='13701087609', updateTime=1785897128388, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709436255555700, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404681641713991, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709436255555701, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404681641713991, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=932, endPage=936, ext={EN=ArticleExt(id=1291404691607380333, articleId=1291404690055487852, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Protective effects of Angelicae and Astragalus ultra-filtration on radiation-induced myocardial cell injury based on NLRP3 inflammasome, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the protective effects of Angelicae and Astragalus ultra-filtration (AAU) on H9C2 myocardial cell injury induced by X-ray radiation based on NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome.
Methods The H9C2 myocardial cells were divided into blank group, model group and experimental -L, -M, -H groups. The H9C2 myocardial cells injury model of model group and experimental -L, -M, -H groups were constructed with X-ray 6 Gy irradiation. After successful modeling, the blank and model groups were treated with 0.9% NaCl; the experimental -L, -M, -H groups were treated with 2%, 5%, 10% AAU drug-containing serum 0.5 mL, respectively. After 24 h of treatment, EdU staining was used to observe cell survival rate, Western blot was used to detect the expression levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and Caspase-1 protein.
Results The cell viability rates of the experimental -M, -H groups, model group and blank group were (89.91±1.16)%, (91.66±1.93)%, (78.61±1.30)% and (98.10±0.20)%; the relative expression levels of NLRP3 protein were 0.79±0.05, 0.74±0.04, 0.94±0.02 and 0.53±0.12; the relative expression levels of ASC protein were 0.40±0.04, 0.41±0.07, 0.48±0.01 and 0.22±0.02; the relative expression levels of Caspase-1 protein were 0.25±0.03, 0.23±0.01, 0.58±0.04 and 0.18±0.01; the relative expression levels of IL-18 protein were 0.67±0.03, 0.62±0.02, 0.91±0.07 and 0.61±0.03; the relative expression levels of IL-1β protein were 0.41±0.06, 0.38±0.02, 0.78±0.02 and 0.34±0.09, respectively. Compared with the experimental -M, -H groups, the differences of above indicators in the model group were statistically significant (all P<0.05).
Conclusion AAU may protect H9C2 myocardial cells from injury induced by X-ray radiation by regulating NLRP3 inflammasome.
, authors=Shu-ling LI
1, Xiao-gang ZHANG
2, Xu-yong WANG
2, Xiao-dong XU
1, authorsList=Shu-ling LI, Xiao-gang ZHANG, Xu-yong WANG, Xiao-dong XU, authorCompany=null, correspAuthors=Xiao-dong XU, 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=1291404693318656366, articleId=1291404690055487852, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于NLRP3炎症小体探讨当归红芪超滤物对放射性心肌细胞损伤的保护作用, 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 基于NOD样受体热蛋白结构域相关蛋白3（NLRP3）炎症小体探讨当归红芪超滤物（AAU）对X线辐射致H9C2心肌细胞损伤的保护作用。
方法 将H9C2心肌细胞分为空白组、模型组和低、中、高剂量实验组。模型组和低、中、高剂量实验组用X射线6 Gy照射构建H9C2心肌细胞损伤模型。建模成功后，模型组和空白组均给予0.9% NaCl处置，低、中、高剂量实验组分别给予2%、5%、10% AAU含药血清0.5 mL进行培养。培养24 h后，用EdU染色法观察细胞存活率，用蛋白质印迹法检测NLRP3、焦亡相关斑点样蛋白（ASC）、胱天蛋白酶-1（Caspase-1）等蛋白的表达水平。
结果 中、高剂量实验组和模型组、空白组的细胞存活率分别为（89.91±1.16）%、（91.66±1.93）%、（78.61±1.30）%和（98.10±0.20）%，NLRP3蛋白相对表达水平分别为0.79±0.05、0.74±0.04、0.94±0.02和0.53±0.12，ASC蛋白相对表达水平分别为0.40±0.04、0.41±0.07、0.48±0.01和0.22±0.02，Caspase-1蛋白相对表达水平分别为0.25±0.03、0.23±0.01、0.58±0.04和0.18±0.01，IL-18蛋白相对表达水平分别为0.67±0.03、0.62±0.02、0.91±0.07和0.61±0.03，IL-1β蛋白相对表达水平分别为0.41±0.06、0.38±0.02、0.78±0.02和0.34±0.09。模型组的上述指标与中、高剂量实验组相比，在统计学上差异均有统计学意义（均P<0.05）。
结论 AAU可能通过调节NLRP3炎症小体对X线辐射导致的H9C2心肌细胞损伤具有保护作用。
, authors=李淑玲
1, 张晓刚
2, 王旭勇
2, 徐晓东
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