Article(id=1291705009280934153, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.20.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1749657600000, receivedDateStr=2025-06-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896072931, onlineDateStr=2026-08-05, pubDate=1761580800000, pubDateStr=2025-10-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896072931, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896072931, creator=13701087609, updateTime=1785896072931, updator=13701087609, issue=Issue{id=1291704786705993936, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='20', pageStart='2851', pageEnd='3000', issueExtLink='null', onlineDate='null', pubDate='1761580800000', pubDateStr='2025-10-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896019864, creator='13701087609', updateTime=1785896741492, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707813508702571, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707813508702572, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704786705993936, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2906, endPage=2911, ext={EN=ArticleExt(id=1291705009469677834, articleId=1291705009280934153, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of berberine improving insulin resistance and liver fat metabolism in obesity mice by regulating PI3K/AKT signaling through miR-125a, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the molecular mechanism of berberine in improving insulin resistance and liver lipid metabolism in obesity mice.
Methods Sixty clean-grade C57BL/6 mice were randomly divided into control group (normal diet), model group (high fat diet), experimental-L group (model+50.00 mg·kg-1 berberine), experimental-H group (model+100.00 mg·kg-1 berberine), inhibitor NC group (model +100.00 mg·kg-1 berberine + tail vein injection mmu-inhibitor NC), miR-125a inhibitor group (model +100.00 mg·kg-1 berberine + tail vein injection of mmu-miR-125a inhibitor). Berberine was administered by gavage once a day, and subcutaneous injection was performed every 4 days. After a continuous treatment period of 28 days, the insulin resistance levels were detected, serum lipid levels were analyzed, the expression levels of related genes were detected by real-time quantitative polymerase chain reaction (RT-qPCR), and the expression of related proteins in liver tissue was detected by Western blot (WB).
Results The levels homeostatis model assessment of insulin resistance (HOMA-IR) in control group, model group, experimental-H group, inhibitor NC group and miR-125a inhibitor group were 2.56±0.11, 7.23±0.67, 5.04±0.20, 4.99±0.34 and 6.46±0.40, respectively; triglyceride (TG) levels were (0.46±0.04), (0.93±0.08), (0.65±0.05), (0.63±0.06) and (0.74±0.06) mmol·L-1, respectively; the relative expression levels of miR-125a were 1.00±0.12, 0.56±0.07, 0.77±0.10, 0.78±0.11 and 0.21±0.03, respectively; fatty acid synthase (FAS) mRNA were 1.00±0.10, 1.90±0.14, 1.40±0.22, 1.41±0.16 and 1.67±0.14, respectively; the relative protein expression levels of phosphorylated phosphatidylase 3-kinase (p-PI3K) were 0.78±0.09, 0.42±0.05, 0.69±0.06, 0.70±0.03 and 0.51±0.06, respectively; phosphorylated protein kinase B (p-AKT) protein levels were 0.84±0.12, 0.30±0.05, 0.64±0.08, 0.65±0.08 and 0.49±0.07, respectively. Compared between the model group and the control group; between the experimental-H group and the model group; and between the miR-125a inhibitor group and the inhibitor NC group, all differences of the above inclicatovs went statistically significant (P<0.01, P<001).
Conclusion Berberine may improve insulin resistance and fat metabolism in obesity mice by activating PI3K/AKT signal through miR-125a.
, authors=Ke MENG
1, Dong YIN
2, Ya-bing LI
1, Jia-rui LI
1, Li-kun DU
1, 3, authorsList=Ke MENG, Dong YIN, Ya-bing LI, Jia-rui LI, Li-kun DU, authorCompany=null, correspAuthors=Li-kun DU, 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=1291705009801027851, articleId=1291705009280934153, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=小檗碱通过
miR-125
a调控PI3K/AKT信号改善肥胖小鼠胰岛素抵抗和肝脂质代谢的研究, 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 探讨小檗碱改善肥胖小鼠胰岛素抵抗和肝脂质代谢的分子机制。
方法 将60只清洁级C57BL/6小鼠随机分为对照组（普通饲料）、模型组（高脂饲料）、低剂量实验组（模型+50.00 mg·kg-1的小檗碱）、高剂量实验组（模型+100.00 mg·kg-1的小檗碱）、inhibitor NC组（模型+100.00 mg·kg-1的小檗碱+尾静脉注射mmu-inhibitor NC），miR-125a inhibitor组（模型+100.00 mg·kg-1的小檗碱+尾静脉注射mmu-miR-125a inhibitor），小檗碱一天灌胃1次，皮下注射每隔4 d 1次，连续治疗28 d后检测胰岛素抵抗水平、用全自动生化分析血清血脂指标水平，实时定量聚合酶链式反应（RT-qPCR）实验检测相关基因表达水平，蛋白质印迹（WB）实验检测肝组织相关蛋白表达。
结果 对照组、模型组、高剂量实验组、inhibitor NC组和miR-125a inhibitor组胰岛素抵抗水平（HOMA-IR）分别为2.56±0.11、7.23±0.67、5.04±0.20、4.99±0.34及6.46±0.40；甘油三酯（TG）水平分别为（0.46±0.04）、（0.93±0.08）、（0.65±0.05）、（0.63±0.06）及（0.74±0.06）mmol·L-1；miR-125a相对表达水平分别为1.00±0.12、0.56±0.07、0.77±0.10、0.78±0.11及0.21±0.03；脂肪酸合成酶（FAS）mRNA水平分别为1.00±0.10、1.90±0.14、1.40±0.22、1.41±0.16及1.67±0.14；磷酸化-磷脂酰化醇3-激酶（p-PI3K）蛋白水平分别为0.78±0.09、0.42±0.05、0.69±0.06、0.70±0.03及0.51±0.06；磷酸化-蛋白质激酶B（p-AKT）蛋白水平分别为0.84±0.12、0.30±0.05、0.64±0.08、0.65±0.08及0.49±0.07；模型组上述指标与对照组比较，高剂量实验组上述指标与模型组比较，miR-125a inhibitor组上述指标与inhibitor NC组比较，在统计学上差异均具有统计学意义（P<0.01，P<001）。
结论 小檗碱可能通过miR-125a激活PI3K/AKT信号改善肥胖小鼠胰岛素抵抗和肝脏脂质代谢。
, authors=孟珂
1, 尹东
2, 李雅冰
1, 李佳睿
1, 杜丽坤
1, 3, authorsList=孟珂, 尹东, 李雅冰, 李佳睿, 杜丽坤, authorCompany=null, correspAuthors=杜丽坤, authorNote=
孟珂（1999年-），女，硕士研究生，主要从事中医药治疗内分泌及代谢性疾病方面的研究
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1.Graduate School of Heilongjiang University of Chinese Medicine, Harbin 150000, Heilongjiang Province, China
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1.黑龙江中医药大学 研究生院，黑龙江 哈尔滨 150000
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