Article(id=1276976078811960313, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251011.709, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1758470400000, receivedDateStr=2025-09-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384422256, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384422256, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384422256, creator=13701087609, updateTime=1782384422256, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=341, endPage=348, ext={EN=ArticleExt(id=1276976079290110970, articleId=1276976078811960313, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Advantageous therapeutic pathways and mechanisms of Jianpi Huogu Formula in treating steroid-induced osteonecrosis of femoral head based on multi-source heterogeneous data integration of disease-syndrome-formula framework, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Based on integrated analysis of multi-source heterogeneous biomedical data combined with animal experimental validation, this study systematically explored the advantageous therapeutic pathways and molecular mechanisms of Jianpi Huogu Formula (JPHGF) in treating steroid-induced osteonecrosis of the femoral head (SONFH). First, the candidate active components and targets of JPHGF were obtained from the Encyclopedia of Traditional Chinese Medicine (ETCM v 2.0). Meanwhile, the Human Phenotype Ontology (HPO) database was used to identify potential genes associated with the corresponding syndrome pattern. Finally, clinical transcriptomic data were analyzed to obtain relevant targets for the phlegm-blood stasis blocking collateral syndrome of SONFH. The intersection of these three types of targets was used to construct a multidimensional "drug-ingredient-disease-syndrome" network. The STRING database was employed for protein-protein interaction (PPI) network analysis, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of core targets was performed via the DAVID platform to predict key biological processes and signaling pathways. Pharmacodynamic and mechanistic validation was subsequently conducted using a rat model of SONFH with phlegm-blood stasis obstructing collateral syndrome. Data integration and mining yielded a "disease and syndrome geneformula and drug target" network containing 146 core targets. Pathway enrichment analysis indicated that JPHGF primarily regulates lipid-coupled intervention in the SONFH phlegm-blood stasis blocking collateral phenotype through the purinergic receptor P2Y12 (P2RY12) -phosphoinositide 3-kinase (PI3K) -serine/threonine kinase (Akt) -fibrinogen gamma chain (FGG) signaling pathway. Hematoxylin-eosin (HE) staining revealed that rats with SONFH of the phlegm-blood stasis blocking collateral type exhibited reduced calcification in femoral head tissues, loosely arranged trabeculae, hypoplastic osteocytes, significantly increased lacunae, and elevated numbers of intramedullary adipocytes. Lipid profile analysis showed elevated triglyceride, total cholesterol, and low-density lipoprotein (LDL) levels, along with decreased high-density lipoprotein (HDL). Coagulation assays demonstrated shortened activated partial thromboplastin time (APTT) and prothrombin time (PT), as well as prolonged thrombin time (TT) and increased plasma fibrinogen levels. Immunohistochemical staining showed that compared with the normal group, the model group exhibited significantly increased positive expression areas of P2RY12, phosphorylated PI3K (p-PI3K), phosphorylated Akt (p-Akt), and FGG proteins in femoral head tissues (P<0.05). In contrast, all drug-treated groups showed significantly reduced expression of these proteins (P<0.05), with the most pronounced inhibitory effect observed in the high-dose group. These results indicate that JPHGF modulates the P2RY12-PI3K-Akt-FGG signaling axis in a dose-dependent manner. In conclusion, JPHGF exerts a syndrome-specific therapeutic effect through multi-target and multi-pathway synergistic actions. By particularly suppressing the excessive activation of the P2RY12-PI3K-Akt-FGG signaling axis, it improves lipid and bone metabolism abnormalities in SONFH with phlegm-blood stasis blocking collateral syndrome.

, authors=null, authorsList=Tao LI, Chu ZHANG, Yan JIA, Wei-heng CHEN, Na LIN, Yan-qiong ZHANG, authorCompany=null, correspAuthors=Na LIN, Yan-qiong 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=1276976079772455933, articleId=1276976078811960313, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于病-证-方多源异构数据整合探索健脾活骨方治疗激素性股骨头坏死的优势环节及其作用机制, columnId=1276976066719781817, journalTitle=中国中药杂志, columnName=股骨头坏死动态血瘀新知及其系统干预前沿专题, runingTitle=null, highlight=null, articleAbstract=

该研究基于多源异构生物医学数据整合分析，并结合动物实验验证，系统探讨健脾活骨方治疗激素性股骨头坏死（SONFH）的优势作用环节及其分子机制。研究首先通过中医药百科全书（ETCM v 2.0）获取健脾活骨方所含候选活性成分及靶点；同时借助HPO数据库挖掘该证候的潜在关联基因；最后，运用临床转录组学检测获取SONFH痰瘀阻络证的相关靶点。对上述三类靶点取交集后，构建“中药-成分-疾病-证候”多维网络。利用STRING数据库进行蛋白质-蛋白质相互作用（PPI）网络分析，并通过DAVID平台对核心靶点进行京都基因与基因组百科全书（KEGG）通路富集分析，以预测其关键生物学过程与信号通路。最后，通过制备SONFH痰瘀阻络证大鼠模型进行药效学和机制验证。经数据整合挖掘获得包含146个网络核心靶标的“病证基因-方药靶标”网络，通路富集分析表明，健脾活骨方主要通过嘌呤能受体P2Y12（P2RY12）-磷脂酰肌醇3-激酶（PI3K）-丝氨酸／苏氨酸激酶（Akt）-纤维蛋白原γ链（FGG）信号通路，调节血脂偶联干预SONFH痰瘀阻络表型。HE染色结果发现，SONFH痰瘀阻络证大鼠的股骨头组织钙化比列降低，骨小梁排列松散，骨细胞欠饱满，空骨陷窝增多明显，骨髓内脂肪细胞增多；血脂四项检测表明，SONFH痰瘀阻络证大鼠甘油三酯、总胆固醇、低密度脂蛋白升高，高密度脂蛋白降低；凝血四项检测表明，SONFH痰瘀阻络证大鼠活化部分凝血活酶时间、凝血酶原时间降低，凝血酶时间和血浆纤维蛋白原升高。免疫组织化学染色结果显示，与正常组比较，模型组大鼠股骨头组织中P2RY12、磷酸化PI3K（p-PI3K）、磷酸化Akt（p-Akt）和FGG蛋白的阳性表达面积显著增加（P<0.05）；而各给药组上述蛋白表达均显著降低（P<0.05），且高剂量组抑制效果最为明显，表明健脾活骨方能够剂量依赖性地调控P2RY12-PI3K-Akt-FGG信号轴。综上所述，健脾活骨方可通过多靶点、多通路协同作用，尤其是抑制P2RY12-PI3K-Akt-FGG信号轴的过度激活，改善SONFH痰瘀阻络证的血脂及骨代谢异常，发挥对证治疗作用。

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