Article(id=1291404584010903694, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.06.017, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1728662400000, receivedDateStr=2024-10-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824445965, onlineDateStr=2026-08-04, pubDate=1743091200000, pubDateStr=2025-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824445965, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824445965, creator=13701087609, updateTime=1785824445965, 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=840, endPage=845, ext={EN=ArticleExt(id=1291404585797677199, articleId=1291404584010903694, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on soyisoflavones alleviate polycystic ovary syndrome in rats by modulating the
miR-29
a-3
p/IGF1 molecular axis, 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 soyisoflavones (SIF) alleviate the rats with polycystic ovary syndrome (PCOS) by regulating the miR-29a-3p/insulin-like growth factor 1 (IGF1) molecular axis.
Methods The female SD rats were divided into normal, model and experimental groups, with 12 rats in each group. The model and experimental groups were induced with gavage letrozole to construct the PCOS rat model. After successful modeling, the normal and model groups were given 100 mg·kg-1 cellulose sodium carboxymethyl by gavage, and the experimental group was given 100 mg·kg-1 SIF by gavage. Three groups were treated for 21 d with once a day. The apoptosis rate of ovarian tissues was detected by TdT-mediated dUTP nick-end labeling, the serum sex hormone levels were detected by enzyme-linked immunosorbnent assay, the expression levels of miR-29a-3p and IGF1 were detected by real-time fluorescence quantitative plymerase chain reaction, and the positive expression level of IGF1 was detected by immunohistochemistry in ovarian tissues. Ovarian granulosa cells from PCOS model rats were divided into blank group (normal culture), experimental group (100 μg·L-1 SIF), miR-29a-3p group (after transfection with miR-29a-3p inhibitor, 100 μg·L-1 SIF culture was given) and IGF1 group (after transfection with miR-29a-3p inhibitor and si-IGF1, 100 μg·L-1 SIF culture was given). Apoptosis of ovarian granulosa cells was measured by mitochondrial membrane potential analysis, and the expression level of apoptosis-related proteins was detected by Western blotting.
Results In the animal experiments, the apoptosis rates of experimental, model and normal groups were (16.14±4.09)%, (23.75±5.68)% and (10.83±3.54)%; the luteinizing hormone levels were (26.81±5.99), (41.55±9.84) and (17.63±3.19) mU·mL-1; the follicle stimulating hormone levels were (51.09±8.72), (41.66±9.87) and (67.91±18.58) pg·mL-1; the relative expression levels of miR-29a-3p were 0.89±0.08, 0.47±0.06 and 1.00±0.11; the relative expression levels of IGF1 mRNA were 1.42±0.39, 2.36±0.54 and 1.00±0.07; the positive expression levels of IGF1 were 1.37±0.31, 1.98±0.41 and 1.00±0.12, respectively. The differences of above indexes in the experimental and normal groups were statistically different from those in the model group (all P<0.05). In the cell experiments, the mitochondrial membrane potentials of the experimental, miR-29a-3p, IGF1 and blank groups were 1.28±0.13, 0.66±0.05, 1.47±0.19 and 0.54±0.06; the relative expressions levels of the B-cell lymphoma-2-associated X protein were 0.73±0.06, 0.97±0.11, 0.62±0.07 and 1.00±0.08; the relative expression levels of B-cell lymphoma-2 were 1.74±0.23, 1.14±0.18, 2.11±0.37 and 1.00±0.05, respectively. The differences of above indexes in the experimental and IGF1 groups were statistically different from those in the miR-29a-3p group (all P<0.05).
Conclusion SIF may delay the progression of PCOS rats by regulating miR-29a-3p/IGF1 pathway to mediate the apoptotic process in ovarian cells.
, authors=Cheng-yong LEI, Li LI, Zhao-xia LUO, Ying HUANG, Qing FENG, Yu LIAN, authorsList=Cheng-yong LEI, Li LI, Zhao-xia LUO, Ying HUANG, Qing FENG, Yu LIAN, authorCompany=null, correspAuthors=Cheng-yong LEI, 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=1291404586552651920, articleId=1291404584010903694, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=大豆异黄酮通过调节
miR-29
a-3
p/IGF1分子轴缓解大鼠多囊卵巢综合征的研究, 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 探讨大豆异黄酮（SIF）通过调节miR-29a-3p/胰岛素样生长因子1（IGF1）分子轴缓解大鼠多囊卵巢综合征（PCOS）的机制。
方法 将雌性SD大鼠分为正常组、模型组和实验组，每组12只。模型组和实验组均灌胃来曲唑诱导构建PCOS大鼠模型。待建模成功后，正常组和模型组均灌胃给予100 mg·kg-1羧甲基纤维素钠溶液，实验组灌胃给予100 mg·kg-1 SIF。3组大鼠每天给药1次，连续21 d。用原位末端转移酶标记法检测卵巢组织中颗粒细胞的凋亡率，用酶联免疫吸附试验法检测血清性激素水平，用实时荧光定量聚合酶链反应检测卵巢组织中miR-29a-3p和IGF1的表达水平，用免疫组化法检测卵巢组织中IGF1阳性表达水平。取PCOS模型大鼠的卵巢颗粒细胞，分为空白组（正常培养）、实验组（100 μg·L-1 SIF）、miR-29a-3p组（转染miR-29a-3p inhibitor后，给予100 μg·L-1 SIF培养）和IGF1组（转染miR-29a-3p inhibitor和si-IGF1后，给予100 μg·L-1 SIF培养）。用线粒体膜电位法检测卵巢颗粒细胞的凋亡情况，用蛋白质印迹法检测凋亡相关蛋白的表达水平。
结果 在动物实验中，实验组、模型组和正常组的细胞凋亡率分别为（16.14±4.09）%、（23.75±5.68）%和（10.83±3.54）%，黄体生成素水平分别为（26.81±5.99）、（41.55±9.84）和（17.63±3.19）mU·mL-1，促卵泡激素水平分别为（51.09±8.72）、（41.66±9.87）和（67.91±18.58）pg·mL-1，miR-29a-3p相对表达水平分别为0.89±0.08、0.47±0.06和1.00±0.11，IGF1 mRNA相对表达水平分别为1.42±0.39、2.36±0.54和1.00±0.07，IGF1阳性表达水平分别为1.37±0.31、1.98±0.41和1.00±0.12。实验组和正常组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。在细胞实验中，实验组、miR-29a-3p组、IGF1组和空白组的线粒体膜电位分别为1.28±0.13、0.66±0.05、1.47±0.19和0.54±0.06，B淋巴细胞瘤-2基因相关X蛋白相对表达水平分别为0.73±0.06、0.97±0.11、0.62±0.07和1.00±0.08，B淋巴细胞瘤-2基因蛋白相对表达水平分别为1.74±0.23、1.14±0.18、2.11±0.37和1.00±0.05。实验组和IGF1组的上述指标与miR-29a-3p组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 SIF可能通过调控miR-29a-3p/IGF1通路介导卵巢细胞的凋亡过程来延缓大鼠PCOS的进展。
, authors=雷承泳, 李丽, 罗朝霞, 黄颖, 冯清, 连瑜, authorsList=雷承泳, 李丽, 罗朝霞, 黄颖, 冯清, 连瑜, authorCompany=null, correspAuthors=雷承泳, authorNote=
雷承泳（1988-），男，主管检验师，主要从事生殖医学方面的临床诊疗工作
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