Article(id=1292126447284539717, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.02.004, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1754496000000, receivedDateStr=2025-08-07, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996551580, onlineDateStr=2026-08-06, pubDate=1769529600000, pubDateStr=2026-01-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996551580, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996551580, creator=13701087609, updateTime=1785996551580, updator=13701087609, issue=Issue{id=1292126409196064779, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='2', pageStart='151', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1769529600000', pubDateStr='2026-01-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996542500, creator='13701087609', updateTime=1786014671444, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202447569707674, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202447569707675, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126409196064779, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=171, endPage=177, ext={EN=ArticleExt(id=1292126447473283398, articleId=1292126447284539717, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of effects of hyperoside on insulin resistance in polycystic ovary syndrome rats by regulating AMPK/GSK3β signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the effect of hyperoside on insulin resistance in polycystic ovary syndrome rats by regulating adenosine monophosphate activated protein kinase (AMPK)/glycogen synthase kinase 3β (GSK3β) signaling pathway.
Methods Nine female SD rats were randomly selected from 45 as the normal (NC) group (equal amount of distilled water), while the rest were used to construct a polycystic ovary syndrome model and grouped into model group (equal amount of distilled water), experimental-L group (0.7 mg·kg-1·d-1 hyperoside), experimental-H group (1.5 mg·kg-1·d-1 hyperoside), and inhibitor group (1.5 mg·kg-1·d-1 hyperoside and 0.2 mg·kg-1·d-1 Compound C), with nine rats in each group. The blood glucose meter was used to measure fasting blood glucose (FBG) in rats. Enzyme linked immunosorbent assay (ELISA) method was used to measure fasting insulin (FINS), testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol (E2), triglycerides (TG), cholesterol (CHO), low-density lipoprotein (LDL), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Hematoxylin-eosin (HE) staining was used to detect pathological changes in ovarian tissue. Western blot was used to measure AMPK/GSK3β signaling pathway proteins in ovarian tissue.
Results The serum FBG levels in NC group, model group, experimental-L group, experimental-H group and inhibitor group were (5.54±0.69), (7.32±0.91), (6.65±0.82), (5.97±0.72) and (6.98±0.85) mmol·L-1, respectively; the serum FINS levels were (9.58±1.39), (15.87±1.96), (13.65±1.62), (11.42±1.57) and (15.04±1.85) mU·L-1, respectively; HOMA-IR indexes were 2.36±0.43, 5.16±0.71, 4.03±0.47, 3.03±0.52 and 4.67±0.68, respectively; the serum TG levels were (0.68±0.09), (1.58±0.18), (1.27±0.17), (0.98±0.13) and (1.46±0.18) mmol·L-1, respectively; the serum CHO levels were (0.76±0.09), (1.52±0.18), (1.24±0.16), (1.01±0.14) and (1.41±0.17) mmol·L-1, respectively; serum LDL levels were (1.62±0.23), (3.59±0.46), (3.06±0.42), (2.54±0.31) and (3.38±0.44) mmol·L-1, respectively; serum LH levels were (4.21±0.57), (9.48±1.39), (7.86±0.96), (6.25±0.74) and (8.87±1.18) ng·mL-1, respectively; serum FSH levels were (19.38±2.52), (8.27±1.05), (11.36±1.42), (14.65±1.76) and (9.57±1.48) ng·mL-1, respectively; the serum T levels were (6.82±0.95), (13.86±1.62), (11.39±1.48), (8.98±1.14) and (12.64±1.53) ng·mL-1, respectively; serum E2 levels were (1.02±0.14), (0.48±0.07), (0.72±0.09), (0.95±0.13) and (0.61±0.08) ng·mL-1, respectively; the serum IL-6 levels were (53.46±7.69), (123.58±18.32), (98.39±13.58), (74.58±9.37) and (114.27±14.72) pg·mg-1, respectively; serum TNF-α levels were (43.74±6.82), (82.19±10.46), (66.39±8.27), (51.72±7.24) and (73.54±1.02) pg·mg-1, respectively; the relative protein expression levels of p-AMPK/AMPK in ovarian tissues were 0.79±0.11, 0.27±0.04, 0.49±0.07, 0.71±0.09 and 0.38±0.06, respectively; the relative protein expression levels of p-GSK3β/GSK3β were 0.19±0.04, 0.68±0.09, 0.47±0.07, 0.28±0.04 and 0.59±0.08, respectively. Among the above indexes, there were all statistically significant differences between NC group and modell group, model group and experimental-L group, experimental-L group and experimental-H group, experimental-H group and inhibitor group (all P<0.05).
Conclusion Hyperoside improves insulin resistance in polycystic ovary syndrome rats by regulating AMPK/GSK3β signaling pathway.
, authors=Ai-ping ZHANG
1, De-xiong ZHAO
2, Ling XIE
3, Chun-xia HUO
3, authorsList=Ai-ping ZHANG, De-xiong ZHAO, Ling XIE, Chun-xia HUO, authorCompany=null, correspAuthors=Ling XIE, 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=1292126447691387207, articleId=1292126447284539717, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=金丝桃苷调节AMPK/GSK3β信号通路对多囊卵巢综合征大鼠胰岛素抵抗影响的研究, 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 探讨金丝桃苷调节腺苷酸活化蛋白激酶（AMPK）/糖原合酶激酶3β（GSK3β）信号通路对多囊卵巢综合征大鼠胰岛素抵抗的影响。
方法 45只雌性SD大鼠中随机选取9只作为正常组，其余均构建多囊卵巢综合征模型，并分为模型组（等量蒸馏水）、低剂量实验组（0.7 mg·kg-1·d-1金丝桃苷）、高剂量实验组（1.5 mg·kg-1·d-1金丝桃苷）和抑制剂组（1.5 mg·kg-1·d-1金丝桃苷+0.2 mg·kg-1·d-1抑制剂Compound C），每组9只。用血糖仪测量大鼠空腹血糖（FBG），用酶联免疫吸附实验（ELISA）测量空腹胰岛素（FINS）、睾酮（T）、促黄体激素（LH）、促卵泡激素（FSH）、雌二醇（E2）、甘油三酯（TG）、胆固醇（CHO）、低密度脂蛋白（LDL）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平，并计算胰岛素抵抗指数（HOMA-IR）；用苏木精-伊红（HE）染色检测卵巢组织病理变化；用蛋白质印迹（Western blot）检测卵巢组织中AMPK/GSK3β信号通路蛋白表达。
结果 正常组、模型组、低剂量实验组、高剂量实验组和抑制剂组大鼠血清FBG水平分别为（5.54±0.69）、（7.32±0.91）、（6.65±0.82）、（5.97±0.72）和（6.98±0.85）mmol·L-1；血清FINS水平分别为（9.58±1.39）、（15.87±1.96）、（13.65±1.62）、（11.42±1.57）和（15.04±1.85）mU·L-1；HOMA-IR指数分别为2.36±0.43、5.16±0.71、4.03±0.47、3.03±0.52、4.67±0.68；血清TG水平分别为（0.68±0.09）、（1.58±0.18）、（1.27±0.17）、（0.98±0.13）和（1.46±0.18）mmol·L-1；血清CHO水平分别为（0.76±0.09）、（1.52±0.18）、（1.24±0.16）、（1.01±0.14）和（1.41±0.17）mmol·L-1；血清LDL水平分别为（1.62±0.23）、（3.59±0.46）、（3.06±0.42）、（2.54±0.31）和（3.38±0.44）mmol·L-1；血清LH水平分别为（4.21±0.57）、（9.48±1.39）、（7.86±0.96）、（6.25±0.74）和（8.87±1.18）ng·mL-1；血清FSH水平分别为（19.38±2.52）、（8.27±1.05）、（11.36±1.42）、（14.65±1.76）和（9.57±1.48）ng·mL-1；血清T水平分别为（6.82±0.95）、（13.86±1.62）、（11.39±1.48）、（8.98±1.14）和（12.64±1.53）ng·mL-1；血清E2水平分别为（1.02±0.14）、（0.48±0.07）、（0.72±0.09）、（0.95±0.13）和（0.61±0.08）ng·mL-1；血清IL-6水平分别为（53.46±7.69）、（123.58±18.32）、（98.39±13.58）、（74.58±9.37）和（114.27±14.72）pg·mg-1；血清TNF-α水平分别为（43.74±6.82）、（82.19±10.46）、（66.39±8.27）、（51.72±7.24）和（73.54±1.02）pg·mg-1；卵巢组织中p-AMPK/AMPK相对蛋白表达水平分别为0.79±0.11、0.27±0.04、0.49±0.07、0.71±0.09和0.38±0.06；p-GSK3β/GSK3β相对蛋白表达水平分别为0.19±0.04、0.68±0.09、0.47±0.07、0.28±0.04和0.59±0.08。正常组与模型组、模型组与低剂量实验组、低剂量实验组与高剂量实验组、高剂量实验组与抑制剂组上述指标比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 金丝桃苷通过调节AMPK/GSK3β信号通路改善多囊卵巢综合征大鼠的胰岛素抵抗。
, authors=张爱萍
1, 赵得雄
2, 谢玲
3, 霍春霞
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张爱萍（1989-），女，主治医师，从事妊娠期高血压疾病的临床工作和研究
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