Article(id=1292135405390946839, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.11.007, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1770220800000, receivedDateStr=2026-02-05, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998687360, onlineDateStr=2026-08-06, pubDate=1781625600000, pubDateStr=2026-06-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998687360, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998687360, creator=13701087609, updateTime=1785998687360, updator=13701087609, issue=Issue{id=1292135402790482407, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='11', pageStart='1501', pageEnd='1650', issueExtLink='null', onlineDate='null', pubDate='1781625600000', pubDateStr='2026-06-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785998686739, creator='13701087609', updateTime=1786014315540, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292200954833686587, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292200954833686588, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135402790482407, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1538, endPage=1544, ext={EN=ArticleExt(id=1292135408305988121, articleId=1292135405390946839, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Pachymic acid prevents cholesterol gallstones by activating the PPARγ/LXRα pathway to regulate hepatic cholesterol metabolism, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of pachymic acid (Pac) on cholesterol metabolism in a gallstone (GS) model and its underlying molecular mechanisms.
Methods A mouse model of GS was established by feeding a high-fat diet. Fifty healthy SPF male mice were randomly divided into five groups: Control group (fed a normal diet), model group (gallstone model), experimental-L group (model + 25 mg·kg-1 Pac), experimental-H group (model+50 mg·kg-1 Pac), and inhibitor group (model + 50 mg·kg-1 Pac + 1 mg·kg-1 GW9662). Gallstone grades were determined based on macroscopic cholesterol crystals or stones observed in bile. The expression of proteins in the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) pathway was detected by Western blot.
Results The gallstone grades in the control, model, experimental-L, experimental-H, and inhibitor groups were (0±0), (4.70±0.46), (3.70±0.64), (1.10±0.70), and (3.20±0.60) grades, respectively; The relative expression levels of PPARγ protein were 1.41±0.13, 0.32±0.02, 0.48±0.05, 1.39±0.15, and 0.80±0.07, respectively; The relative expression levels of LXRα protein were 0.99±0.07, 0.33±0.03, 0.42±0.02, 1.00±0.09, and 0.73±0.05, respectively. Statistically significant differences were observed when comparing the model group with the control, experimental-L, and experimental-H groups, as well as when comparing the inhibitor group with the experimental-H group (all P<0.05).
Conclusion Pachymic acid effectively prevents high-fat diet-induced cholesterol gallstone formation in mice. Its protective mechanism is associated with the activation of the PPARγ/LXRα signaling pathway, leading to the restoration of cholesterol metabolic homeostasis.
, authors=Qing-xiang ZHANG, Qian WU, Jian-xiong TAI, Ning LI, Guang LI, Zhao-ming LIU, Heng-li LI, authorsList=Qing-xiang ZHANG, Qian WU, Jian-xiong TAI, Ning LI, Guang LI, Zhao-ming LIU, Heng-li LI, authorCompany=null, correspAuthors=Qing-xiang ZHANG, 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=1292135409501364762, articleId=1292135405390946839, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=茯苓酸通过激活PPARγ/LXRα通路调节胆固醇代谢防治胆结石的机制研究, 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 探讨茯苓酸（Pac）对胆结石（GS）模型胆固醇代谢的影响及其潜在分子机制。
方法 通过饲喂高脂饲料构建GS小鼠模型。将50只健康SPF级雄性小鼠随机分为对照组（普通饮食）、模型组（建模）、低剂量实验组（建模+25 mg·kg-1 Pac）、高剂量实验组（建模+50 mg·kg-1 Pac）和抑制剂组（建模+50 mg·kg-1 Pac+1 mg·kg-1 GW9662）。对胆汁中肉眼可见的胆固醇结晶或结石进行胆结石等级测定。蛋白质印迹法检测过氧化物体增生物激活受体γ（PPAR γ）/肝X受体α（LXRα）通路蛋白的表达。
结果 对照组、模型组、低剂量实验组、高剂量实验组和抑制剂组的小鼠的胆结石等级分别为（0±0）、（4.70±0.46）、（3.70±0.64）、（1.10±0.70）和（3.20±0.60）级，PPARγ蛋白相对表达水平分别为1.41±0.13、0.32±0.02、0.48±0.05、1.39±0.15和0.80±0.07，LXRα蛋白相对表达水平分别为0.99±0.07、0.33±0.03、0.42±0.02、1.00±0.09和0.73±0.05。模型组的上述指标与对照组、低剂量实验组、高剂量实验组比较，抑制剂组的上述指标与高剂量实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 Pac能够有效预防高脂饮食诱导的小鼠胆固醇性胆结石形成，其作用机制与激活PPARγ/LXRα信号通路，重塑胆固醇代谢稳态有关。
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张青向（1989-），男，主治医师，主要从事肝胆胰外科方面的研究和工作
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