Article(id=1291404577014796601, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.06.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1730217600000, receivedDateStr=2024-10-30, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824444296, onlineDateStr=2026-08-04, pubDate=1743091200000, pubDateStr=2025-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824444296, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824444296, creator=13701087609, updateTime=1785824444296, updator=13701087609, issue=Issue{id=1291404554201985968, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='6', pageStart='751', pageEnd='900', issueExtLink='null', onlineDate='null', pubDate='1743091200000', pubDateStr='2025-03-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824438858, creator='13701087609', updateTime=1785897146949, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709514101846462, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709514101846463, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=828, endPage=833, ext={EN=ArticleExt(id=1291404577346146618, articleId=1291404577014796601, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the protective effects of bezafibrate on the kidney tissue of mice with diabetic nephropathy, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the mechanism of action of bezafibrate (BEZ) targeting nuclear factor of activated T cells 5 (NFAT5) through microribonucleic acid (miR)-486-5p on the kidney tissues of mice with diabetic nephropathy.
Methods Db/m mice were used as control group. Db/db mice were used to construct a diabetic nephropathy model, which was divided into 4 groups according to the random number table method: Model group, experimental group (75 mg·kg-1·d-1 BEZ), miR-486-5p antagomir group (75 mg·kg-1·d-1 BEZ+10 mg·kg-1 miR-486-5p antagomir), sh-NFAT5 group (75 mg·kg-1·d-1 BEZ+10 mg·kg-1 miR-486-5p antagomir+recombinant adenovirus containing NFAT5 knockdown plasmid). The kit was used to detect the levels of renal function and oxidative stress in mice; and the expression levels of glucose metabolism and renal fibrosis-related proteins in renal tissues of mice in each group were detected by Western blot.
Results The levels of malondialdehyde (MDA) in the control group, model group, experimental group, miR-486-5p antagomir group, and sh-NFAT5 group were (2.78±0.56), (4.96±0.97), (3.02±0.54), (4.51±0.79) and (3.24±0.58) nmol·mg-1, respectively; the levels of aldose reductase (AR) were 1.00±0.12, 3.61±0.43, 1.82±0.29, 3.09±0.58 and 2.25±0.47, respectively; the levels of pyruvate dehydrogenase (PDH) were 1.00±0.11, 0.53±0.10, 0.91±0.15, 0.64±0.12 and 0.82±0.14, respectively; the levels of pyruvate dehydrogenase E1 subunit α1 (PDHA1) were 1.00±0.14, 0.36±0.07, 0.83±0.16, 0.51±0.11 and 0.74±0.13, respectively; the levels of pyruvate dehydrogenase kinase (PDK) were 1.00±0.10, 2.59±0.52, 1.34±0.31, 2.11±0.43 and 1.56±0.39, respectively; the levels of transforming growth factor-β1 (TGF-β1) were 1.00±0.11, 3.15±0.52, 1.43±0.38, 2.72±0.43 and 1.89±0.57, respectively; the levels of fibronectin (FN) were 1.00±0.09, 2.84±0.57, 1.46±0.41, 2.59±0.52 and 1.73±0.49, respectively; the levels of collagen type I (Collagen I) were 1.00±0.13, 4.28±0.71, 2.03±0.46, 3.64±0.68 and 2.51±0.53, respectively. The above indicators of the control group were compared with the model group, the above indicators of the model group were compared with the experimental group, the above indicators of the experimental group were compared with the miR-486-5p antagomir group, and the above indicators of the miR-486-5p antagomir group were compared with the sh-NFAT5 group. The differences were statistically significant (P<0.05, P<0.01, P<0.001).
Conclusion BEZ can effectively protect the kidney tissue of mice with diabetic nephropathy, and the mechanism may be realized through the miR-486-5p/NFAT5 signaling pathway.
, authors=Gen-yan LUO, Lin-fei DONG, Dong-liang YANG, Yuan LIU, Zi-qi YANG, Yan ZHONG, Zhi-jian GONG, authorsList=Gen-yan LUO, Lin-fei DONG, Dong-liang YANG, Yuan LIU, Zi-qi YANG, Yan ZHONG, Zhi-jian GONG, authorCompany=null, correspAuthors=Gen-yan LUO, 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=1291404577669108027, articleId=1291404577014796601, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=苯扎贝特对糖尿病肾病小鼠肾组织的保护作用, 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 探究苯扎贝特（BEZ）通过微小核糖核酸（miR）-486-5p靶向活化T细胞的核因子5（NFAT5）对糖尿病肾病小鼠肾组织的作用机制。
方法 db/m小鼠作为对照组；db/db小鼠构建糖尿病肾病模型，将其按随机数字表法分为模型组、实验组（75 mg·kg-1·d-1BEZ），miR-486-5p antagomir组（75 mg·kg-1·d-1 BEZ + 10 mg kg-1 miR-486-5p antagomir），sh-NFAT5组（75 mg·kg-1·d-1 BEZ + 10 mg kg-1 miR-486-5p antagomir+NFAT5敲低质粒的重组腺病毒。用试剂盒检测小鼠肾功能与氧化应激相关指标水平，用蛋白质印迹法检测各组小鼠肾组织糖代谢和肾纤维化相关蛋白的表达水平。
结果 对照组、模型组、实验组、miR-486-5p antagomir组、sh-NFAT5组的丙二醛水平分别为（2.78±0.56）、（4.96±0.97）、（3.02±0.54）、（4.51±0.79）和（3.24±0.58）nmol·mg-1，醛糖还原酶蛋白相对表达水平分别为1.00±0.12、3.61±0.43、1.82±0.29、3.09±0.58和2.25±0.47，丙酮酸脱氢酶蛋白相对表达水平分别为1.00±0.11、0.53±0.10、0.91±0.15、0.64±0.12和0.82±0.14，丙酮酸脱氢酶E1亚基α1蛋白相对表达水平分别为1.00±0.14、0.36±0.07、0.83±0.16、0.51±0.11和0.74±0.13，丙酮酸脱氢酶激酶蛋白相对表达水平分别为1.00±0.10、2.59±0.52、1.34±0.31、2.11±0.43和1.56±0.39，转化生长因子-β1蛋白相对表达水平分别为1.00±0.11、3.15±0.52、1.43±0.38、2.72±0.43和1.89±0.57，纤连蛋白相对表达水平分别为1.00±0.09、2.84±0.57、1.46±0.41、2.59±0.52和1.73±0.49，Ⅰ型胶原蛋白相对表达水平分别为1.00±0.13、4.28±0.71、2.03±0.46、3.64±0.68和2.51±0.53。对照组的上述指标与模型组比较，模型组的上述指标与实验组比较，实验组的上述指标与miR-486-5p antagomir组比较，miR-486-5p antagomir组的上述指标与sh-NFAT5组比较，在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。
结论 BEZ可有效保护糖尿病肾病小鼠肾组织，其机制可能是通过miR-486-5p/NFAT5信号通路实现的。
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罗根艳（1981-），女，副主任医师，主要从事全科医学、内科方面的临床诊疗工作
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