Article(id=1291339109247742720, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291339070622396983, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.03.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1723219200000, receivedDateStr=2024-08-10, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785808835564, onlineDateStr=2026-08-04, pubDate=1739721600000, pubDateStr=2025-02-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785808835564, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785808835564, creator=13041195026, updateTime=1785808835564, 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=1785808826353, updator='13041195026', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=372, endPage=375, ext={EN=ArticleExt(id=1291339109423903489, articleId=1291339109247742720, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of microRNA-142a-3p mediates adriamycin-induced nephropathy by targeting down-regulation of Atg16l1 expression, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore effect and mechanism of microRNA 142a-3p (miR-142a-3p) on adriamycin-induced nephropathy (AN).
Methods BALB/c mice were randomly divided into normal group and model group. The model group was injected with 10.5 mg·kg-1 doxorubicin at a time through the tail vein, and the normal group was injected with equal volume 0.9% NaCl by the same method. After 28 days of feeding, both sides of the kidney tissues were taken for experiment. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-142a-3p in the renal tissues. The expression levels of autophagy related protein 16-like protein 1 (Atg16l1) and inflammatory NOD-like receptor heat protein domain associated protein 3 (NLRP3), interleukin-1β (IL-1β) and interleukin-18 (IL-18) in the renal tissues were detected by Western blotting. Human embryonic kidney 293T cells were divided into Atg16l1-WT+NC transfection group (transfected pmirGLO-Atg16l1-WT and NC mimics) and Atg16l1-WT+miRNA-142a-3p group (transfected pmirGLO-Atg16l1-WT and miR-142a-3p mimics). Dual luciferase assay was used to detect the targeted regulation of miR-142a-3p on Atg16l1.
Results The expression levels of miR-142a-3p in kidney tissues of normal group and model group were 1.20±0.27 and 2.02±0.14; the expression levels of Atg16l1 were 0.81±0.13 and 0.57±0.12, NLRP3 were 0.49±0.11 and 0.82±0.14; IL-1β were 0.55±0.11 and 0.84±0.08; IL-18 levels were 0.41±0.15 and 0.74±0.09, respectively, and the above indexes in the model group were significantly different from those in the normal group (all P<0.05). The relative luciferase activity in Atg16l1-WT+NC transfection group and Atg16l1-WT+miRNA-142a-3p transfection group were 1.26±0.07 and 0.92±0.10, respectively, with statistical significance (all P<0.05).
Conclusion MiR-142a-3p down-regulates the expression of target protein Atg16l1 in renal tissue of adriamycin nephropathy mice, which activates NLRP3 pathway of inflammatory bodies and promotes the progressive development of adriamycin-induced nephropathy.
, authors=Rui-yang YUAN, Hai-mai DING, Xing ZHAO, Li-de SU, Xue-ming ZHANG, authorsList=Rui-yang YUAN, Hai-mai DING, Xing ZHAO, Li-de SU, Xue-ming ZHANG, authorCompany=null, correspAuthors=Xue-ming 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=1291339109843333890, articleId=1291339109247742720, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=微小RNA-142a-3p通过靶向下调Atg16l1表达介导阿霉素肾病的研究, 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 探究微小RNA-142a-3p（miR-142a-3p）介导阿霉素肾病（AN）的作用机制。
方法 将BALB/c小鼠随机分为正常组与模型组，模型组通过尾静脉一次性注射10.5 mg·kg-1阿霉素；正常组使用相同方法注射等体积0.9% NaCl。饲养28 d后取其两侧肾组织用于后续实验。用实时荧光定量聚合酶链反应（RT-qPCR）检测肾组织中miR-142a-3p表达情况；用蛋白质印迹法检测肾组织中自噬相关蛋白16样蛋白1（Atg16l1）及炎症相关的NOD样受体热蛋白结构域相关蛋白3（NLRP3）、白细胞介素-1β（IL-1β）和白细胞介素-18（IL -18）蛋白的相对表达水平。将人胚肾HEK293T细胞分为Atg16l1-WT+NC转染组（转染pmirGLO-Atg16l1-WT和NC mimics）和Atg16l1-WT+miRNA-142a-3p转染组（转染pmirGLO-Atg16l1-WT和miR-142a-3p mimics）。用双荧光素酶实验检测miR-142a-3p对Atg16l1的靶向调控。
结果 正常组与模型组肾组织中miR-142a-3p的相对表达水平分别为1.20±0.27、2.02±0.14；Atg16l1蛋白的相对表达水平分别为0.81±0.13、0.57±0.12；NLRP3蛋白相对表达水平分别为0.49±0.11、0.82±0.14；IL-1β蛋白相对表达水平分别为0.55±0.11、0.84±0.08；IL-18蛋白相对表达水平分别为0.41±0.15、0.74±0.09，模型组上述指标与正常组比较，在统计学上差异均有统计学意义（均P<0.05）。Atg16l1-WT+NC转染组和Atg16l1-WT+miRNA-142a-3p转染组的相对荧光活性分别为1.26±0.07和0.92±0.10，在统计学上差异均有统计学意义（均P<0.05）。
结论 阿霉素肾病小鼠肾组织中miR-142a-3p下调靶蛋白Atg16l1的表达，激活炎症小体NLRP3通路，促进阿霉素小鼠肾病的进行性发展。
, authors=袁瑞阳, 丁海麦, 赵星, 苏力德, 张学明, authorsList=袁瑞阳, 丁海麦, 赵星, 苏力德, 张学明, authorCompany=null, correspAuthors=张学明, authorNote=
袁瑞阳（1998-），女，硕士研究生，主要从事慢性肾病的相关研究
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