Article(id=1292130355084022189, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.05.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1765987200000, receivedDateStr=2025-12-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997483273, onlineDateStr=2026-08-06, pubDate=1773676800000, pubDateStr=2026-03-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997483273, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997483273, creator=13701087609, updateTime=1785997483273, updator=13701087609, issue=Issue{id=1292130254689165893, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='5', pageStart='601', pageEnd='750', issueExtLink='null', onlineDate='null', pubDate='1773676800000', pubDateStr='2026-03-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997459337, creator='13701087609', updateTime=1786014469153, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201599108141219, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201599108141220, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130254689165893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=650, endPage=656, ext={EN=ArticleExt(id=1292130356233261486, articleId=1292130355084022189, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the effects of curculigoside on aortic dissection rats by inhibiting ROS/NLRP3 pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the ameliorative effects of curculigoside on rats with aortic dissection by the inhibition of the reactive oxygen species /NOD-like receptor thermal protein domain associated protein 3 (ROS/NLRP3) pathway.
Methods Rats were randomly divided into control group, model group, low-dose experimental group (50 mg·kg-1 curculigoside), high-dose experimental group (100 mg·kg-1 curculigoside) and combination group (100 mg·kg-1 curculigoside and 1.75 mg·mL-1 trimethylamine N-oxide), with 12 rats in each group. The rat model of aortic dissection was established by intragastric administration of 0.1 g·kg-1 β-aminopropionitrile (BAPN). Cardiac blood was collected, and the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). hematoxylin-eosin (HE) staining and Van Gieson staining were used to evaluate histopathological changes and the degree of elastic fiber rupture. Reactive oxygen species (ROS) levels were detected using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining. The mRNA expression levels of matrix metalloproteinase 9 (MMP-9) and matrix metalloproteinase 2 (MMP-2) in aortic tissues were measured by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). The protein expression levels of apoptosis-associated speck-like protein containing a CARD (ASC), NLR family pyrin domain-containing 3 (NLRP3) and caspase-1 in aortic tissues were detected by Western blotting.
Results The IL-6 levels in the low-dose experimental group, high-dose experimental group, control group, model group and combination group were (49.06±4.98), (37.18±3.81), (35.62±3.63), (72.34±7.33) and (50.03±5.08) pg·mL-1, respectively; the TNF-α levels were (25.63±2.64), (16.35±1.71), (15.31±1.62), (42.06±4.23) and (26.15±2.64) pg·mL-1, respectively; the degrees of elastic fiber rupture were 2.01±0.22, 0.85±0.09, 0±0, 3.22±0.34 and 1.85±0.19, respectively; the ROS levels were 358.62±36.64, 203.11±20.15, 186.34±19.11, 588.64±60.03 and 361.24±37.24, respectively; the relative mRNA expression levels of MMP-9 were 1.67±0.18, 1.15±0.12, 1.02±0.11, 2.45±0.26 and 1.72±0.19, respectively; the relative mRNA expression levels of MMP-2 were 1.88±0.19, 1.24±0.14, 0.98±0.10, 2.85±0.30 and 1.91±0.20, respectively; the relative protein expression levels of Caspase-1 were 0.85±0.09, 0.55±0.06, 0.44±0.05, 1.24±0.13 and 0.88±0.10, respectively; the relative protein expression levels of ASC were 0.97±0.10, 0.64±0.08, 0.55±0.06, 1.48±0.16 and 0.89±0.09, respectively; and the relative protein expression levels of NLRP3 were 0.64±0.08, 0.35±0.05, 0.25±0.03, 1.02±0.11 and 0.72±0.09, respectively. Compared with the control group, the above indicators in the model group were significantly different (all P<0.05); compared with the model group, the above indicators in the high-dose experimental group were significantly different (all P<0.05); and compared with the high-dose experimental group, the above indicators in the combination group were significantly different (all P<0.05).
Conclusion Curculigoside can effectively ameliorate BAPN-induced aortic injury in rats. Its protective mechanism against the development of aortic dissection may be associated with the inhibition of the ROS/NLRP3 signaling pathway.
, authors=Zhao-yang LI, En-gang WU, Feng WANG, Wei LI, Sheng-jun DONG, Kai-qiang YANG, Ning GAI, authorsList=Zhao-yang LI, En-gang WU, Feng WANG, Wei LI, Sheng-jun DONG, Kai-qiang YANG, Ning GAI, authorCompany=null, correspAuthors=Ning GAI, 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=1292130356736577969, articleId=1292130355084022189, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=仙茅苷抑制ROS/NLRP3通路对主动脉夹层大鼠作用的研究, 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 探讨仙茅苷抑制活性氧/NOD样受体家族含热蛋白结构域蛋白3（ROS/NLRP3）通路对主动脉夹层大鼠的作用。
方法 将60只大鼠随机分为对照组、模型组、低剂量实验组（50 mg·kg-1仙茅苷）、高剂量实验组（100 mg·kg-1仙茅苷）和联合组（100 mg·kg-1仙茅苷+1.75 mg·mL-1三甲胺N-氧化物），每组12只。除对照组外，其余组大鼠均通过灌胃β-氨基丙腈（0.1 g·kg-1）建立主动脉夹层大鼠模型。采集心脏血液，用酶联免疫吸附法（ELISA）测定白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平；用苏木精-伊红染色法（HE）及Van Gieson染液检测组织病理变化及弹性纤维断裂的程度；用双氯荧光素（DCFH-DA）染色法检测活性氧（ROS）水平；用实时定量反转录聚合酶链式反应（qRT-PCR）法检测主动脉组织中金属基质蛋白酶9（MMP-9）信使核糖核酸（mRNA）和金属基质蛋白酶2（MMP-2）mRNA表达；用蛋白质印迹法检测主动脉组织中凋亡相关斑点样蛋白（ASC）、NLRP3和半胱天冬酶-1（Caspase-1）蛋白表达。
结果 低剂量实验组、高剂量实验组、对照组、模型组和联合组的IL-6分别为（49.06±4.98）、（37.18±3.81）、（35.62±3.63）、（72.34±7.33）和（50.03±5.08）pg·mL-1；TNF-α分别为（25.63±2.64）、（16.35±1.71）、（15.31±1.62）、（42.06±4.23）和（26.15±2.64）pg·mL-1；弹性纤维断裂程度分别为2.01±0.22、0.85±0.09、0±0、3.22±0.34和1.85±0.19；ROS分别为358.62±36.64、203.11±20.15、186.34±19.11、588.64±60.03和361.24±37.24；MMP-9 mRNA相对表达水平分别为1.67±0.18、1.15±0.12、1.02±0.11、2.45±0.26和1.72±0.19；MMP-2 mRNA相对表达水平分别为1.88±0.19、1.24±0.14、0.98±0.10、2.85±0.30和1.91±0.20；Caspase-1蛋白相对表达水平分别为0.85±0.09、0.55±0.06、0.44±0.05、1.24±0.13和0.88±0.10；ASC蛋白相对表达水平0.97±0.10、0.64±0.08、0.55±0.06、1.48±0.16和0.89±0.09和NLRP3蛋白相对表达水平分别为0.64±0.08、0.35±0.05、0.25±0.03、1.02±0.11和0.72±0.09。模型组的上述指标与对照组比较，高剂量实验组的上述指标与模型组比较，联合组的上述指标与高剂量实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 仙茅苷能够有效改善β-氨基丙腈大鼠主动脉损伤，可能是通过抑制ROS/NLRP3通路改善主动脉夹层的发生。
, authors=李昭阳, 吴恩刚, 王锋, 李伟, 董圣军, 杨凯强, 盖宁, authorsList=李昭阳, 吴恩刚, 王锋, 李伟, 董圣军, 杨凯强, 盖宁, authorCompany=null, correspAuthors=盖宁, authorNote=
李昭阳（1998-），男，硕士研究生，主要从事主动脉夹层方面的研究
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李昭阳（1998-），男，硕士研究生，主要从事主动脉夹层方面的研究
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