Article(id=1291704939823260452, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.17.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746720000000, receivedDateStr=2025-05-09, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896056340, onlineDateStr=2026-08-05, pubDate=1758038400000, pubDateStr=2025-09-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896056340, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896056340, creator=13701087609, updateTime=1785896056340, updator=13701087609, issue=Issue{id=1291704771212234905, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='17', pageStart='2401', pageEnd='2550', issueExtLink='null', onlineDate='null', pubDate='1758038400000', pubDateStr='2025-09-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896016147, creator='13701087609', updateTime=1785896900366, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708479866164175, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708479866164176, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704771212234905, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2471, endPage=2476, ext={EN=ArticleExt(id=1291704940108473125, articleId=1291704939823260452, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of fucoxanthin targeted
miR-483-3
p expression to improve endothelial cell function in coronary heart disease, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of fucoxanthin on endothelial cell function in coronary heart disease (CHD) and its mechanism.
Methods The cell experiment section divided the human coronary artery endothelial cells (HCAEC) into blank group, ox-LDL group (40 μg·mL-1), fucoxanthin group (ox-LDL+25 μmol·L-1 fucoxanthin) and miR-483-3p inhibitor group (transfected with miR-483-3p inhibitor+ox-LDL+25 μmol·L-1 fucoxanthin). The expression levels of miR-483-3p and pyroptosis related proteins NLR family pyrin domain containing 3 (NLRP3) were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting (WB), respectively. The animal experiment section divided the rats into control group, model group (constructed CHD model), experimental group (modeling +30 mg·kg-1 fucoxanthin) and inhibitor group (modeling+transfection of miR-483-3p inhibitor+30 mg·kg-1 fucoxanthin). The relative expression levels of miR-483-3p, endothelium-related factors and pyroptosis related proteins NLRP3 were detected by RT-qPCR, enzyme-linked immunosorbent assay (ELISA) and Western blot, respectively.
Results In cell experiment, the relative expression levels of miRNA-483-3p in cells of blank group, ox-LDL group, fucoxanthin group and miR-483-3p inhibitor group were 1.00±0.11, 0.39±0.07, 0.74±0.06 and 0.22±0.03, respectively; NLRP3 protein relative expression levels were 0.39±0.02, 1.03±0.07, 0.52±0.04 and 0.85±0.10, respectively. ox-LDL group was compared with blank group, fucoxanthin group was compared with ox-LDL group, miR-483-3p inhibitor group was compared with fucoxanthin group, the above indicators all showed statistically significant differences. (all P<0.001). In animal experiments, the relative expression levels of miR-483-3p in control group, model group, experimental group and inhibitor group were 1.00±0.12, 0.51±0.06, 0.70±0.08 and 0.31±0.04, respectively; nitric oxide (NO) levels were (46.93±3.18), (20.21±2.43), (36.13±4.87) and (24.43±1.60) μmol·L-1, respectively; the NLRP3 protein relative expression levels were 0.29±0.04, 0.97±0.09, 0.56±0.09 and 0.86±0.08, model group was compared with control group, experimental group was compared with model group, inhibitor group was compared with experimental group, the above indicators all showed statistically significant differences. (all P<0.001).
Conclusion Fucoxanthin can up-regulate miR-483-3p to improve endothelial cell pyroptosis and relieve CHD inflammatory response.
, authors=Ling-wei ZENG
1a, Jing YANG
1b, Chang-yi WANG
1a, Liang LI
1a, authorsList=Ling-wei ZENG, Jing YANG, Chang-yi WANG, Liang LI, authorCompany=null, correspAuthors=Ling-wei ZENG, 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=1291704940548875046, articleId=1291704939823260452, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=岩藻黄质靶向调控
miR-483-3
p表达改善冠心病内皮细胞功能研究, 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 探讨岩藻黄质对冠心病(CHD)内皮细胞功能的影响及其作用机制。
方法 在细胞实验部分,将人类冠状动脉内皮细胞(HCAEC)分为空白组、ox-LDL组(40 μg·mL-1)、药物组(ox-LDL+25 μmol·L-1岩藻黄质)和miR-483-3p inhibitor组(转染miR-483-3p inhibitor-+ox-LDL+25 μmol·L-1岩藻黄质);分别用实时荧光定量聚合酶链反应(RT-qPCR)及蛋白免疫印迹(WB)法检测miR-483-3p基因和焦亡相关蛋白含NLR家族pyrin域蛋白3(NLRP3)相对表达水平。在动物实验部分,将大鼠分为对照组、模型组(构建CHD模型)、实验组(建模+30 mg·kg-1岩藻黄质)和抑制剂组(建模+转染miR-483-3p inhibitor+30 mg·kg-1岩藻黄质);分别用RT-qPCR、酶联免疫吸附测定(ELISA)法及WB法检测miR-483-3p相对表达水平、内皮相关因子及焦亡相关蛋白NLRP3相对表达水平。
结果 在细胞实验部分中,空白组、ox-LDL组、药物组和miR-483-3p inhibitor组细胞的miR-483-3p相对表达水平分别为1.00±0.11、0.39±0.07、0.74±0.06和0.22±0.03;NLRP3蛋白相对表达水平分别为0.39±0.02、1.03±0.07、0.52±0.04和0.85±0.10,ox-LDL组与空白组比较,药物组与ox-LDL组比较,miR-483-3p inhibitor组与药物组比较,上述指标在统计学上差异均有统计学意义(均P<0.001)。在动物实验部分中,对照组、模型组、实验组和抑制剂组的miR-483-3p相对表达水平分别为1.00±0.12、0.51±0.06、0.70±0.08和0.31±0.04;一氧化氮(NO)水平分别为(46.93±3.18)、(20.21±2.43)、(36.13±4.87)和(24.43±1.60)μmol·L-1;NLRP3蛋白相对表达水平分别为0.29±0.04、0.97±0.09、0.56±0.09和0.86±0.08,模型组与对照组比较,实验组与模型组比较,抑制剂组与实验组比较,上述指标在统计学上差异均有统计学意义(均P<0.001)。
结论 岩藻黄质可以上调miR-483-3p相对表达水平,改善内皮细胞焦亡,缓解CHD炎性反应。
, authors=曾令伟
1a, 杨晶
1b, 王长义
1a, 李亮
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