Article(id=1317125411016913812, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.03.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791956768993, onlineDateStr=2026-10-14, pubDate=1773072000000, pubDateStr=2026-03-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791956768993, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791956768993, creator=13701087609, updateTime=1791956768993, updator=13701087609, issue=Issue{id=1317125400581485316, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='3', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1773072000000', pubDateStr='2026-03-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791956766504, creator='13701087609', updateTime=1791958763799, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133777898418844, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133777898418845, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=50, endPage=54, ext={EN=ArticleExt(id=1317125411230823317, articleId=1317125411016913812, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Mechanisms of Linggui Zhugan Decoction（苓桂术甘汤）Interfering in PI3K/AKT Pathway to Affect Fatty Acid Metabolism in NAFLD Mice, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect of Linggui Zhugan Decoction（苓桂术甘汤）on lipid metabolism in mice with nonalcoholic fatty liver disease（NAFLD）, and to provide a new target and data support for clinical treatment of NAFLD.
Methods C57BL/6J mice were used as the blank control group. ApoE-/- mice were divided into model group, Linggui Zhugan Decoction low, middle and high dose groups and simvastatin group. The blood lipid levels of mice were detected by automatic biochemical analyzer. Hematoxylin-eosin（HE）staining and oil red O staining were used to determine the degree of liver steatosis in NAFLD mice. RT-qPCR was used to detect the mRNA expressions of PI3K, AKT, FASN, SREBP1 and ATGL. The protein expressions of PI3K, AKT, p-AKT, FASN, SREBP1 and ATGL were detected by Western Blot.
Results After treatment with Linggui Zhugan Decoction, the serum levels of total cholesterol（TC）, triglyceride（TG）and low-density lipoprotein cholesterol（LDL-C）were down-regulated（P < 0.05）. The expressions of fatty acid synthesis related genes and proteins FASN and SREBP1 were decreased（P < 0.05）, and the expressions of TG breakdown related genes and proteins ATGL were increased（P < 0.05）. The protein expressions of PI3K and p-AKT were significantly increased（P < 0.05）.
Conclusion Linggui Zhugan Decoction may inhibit the occurrence and development of NAFLD by promoting the decomposition of hepatic triglyceride and inhibiting fatty acid synthesis through PI3K/AKT signaling pathway.
, authors=Yuan ZHANG
1, Zhuo YANG
1, Yuan CAO
2, Qun WANG
2, authorsList=Yuan ZHANG, Zhuo YANG, Yuan CAO, Qun WANG, authorCompany=null, correspAuthors=Zhuo YANG, 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=1317125411570561942, articleId=1317125411016913812, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=苓桂术甘汤干预PI3K/AKT通路影响脂肪酸代谢减缓小鼠非酒精性脂肪肝的机制研究, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 探讨苓桂术甘汤对非酒精性脂肪肝病（Nonalcoholic fatty liver disease，NAFLD）小鼠脂质代谢的影响，为临床治疗NAFLD提供新的靶点与数据支持。
方法 C57BL/6J小鼠作为空白对照组，将ApoE-/-小鼠分为模型组、苓桂术甘汤低中高剂量组。利用全自动生化分析仪检测小鼠的血脂水平；HE染色与油红O染色判断NAFLD小鼠肝脏脂肪变性程度；RT-qPCR方法检测PI3K、AKT、FASN、SREBP1、ATGL mRNA的表达情况；Western Blot方法检测PI3K、AKT、p-AKT、FASN、SREBP1、ATGL蛋白表达情况。
结果 经苓桂术甘汤治疗后，下调了小鼠血清的TC、TG及LDL-C水平（P < 0.05）；脂肪酸合成相关基因与蛋白FASN与SREBP1表达降低（P < 0.05），TG分解相关基因与蛋白ATGL表达升高（P < 0.05）；PI3K及p-AKT蛋白表达升高（P < 0.05）。
结论 苓桂术甘汤可能通过PI3K/AKT信号通路促进肝脏甘油三酯分解，抑制脂肪酸合成延缓NAFLD发生发展。
, authors=张援
1, 杨卓
1, 曹媛
2, 王群
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张援（1984 -），女，辽宁海城人，副主任医师，硕士，研究方向：中西医结合治疗消化系统疾病。
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