Article(id=1276976066308740022, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250717.402, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1749398400000, receivedDateStr=2025-06-09, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384419276, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384419276, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384419276, creator=13701087609, updateTime=1782384419276, 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=332, endPage=340, ext={EN=ArticleExt(id=1276976066635895736, articleId=1276976066308740022, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Scientific connotation of Jianpi Huogu Formula in treating steroid-induced ONFH based on lipid metabolism reprogramming and transcriptional regulatory network, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study systematically elucidated the scientific connotation of Jianpi Huogu Formula in treating phlegm-stasis blocking collaterals syndrome in steroid-induced osteonecrosis of the femoral head (SONFH) by integrating clinical transcriptomics, lipid metabolomics, and biomolecular network mining techniques. The invigorating the spleen and resolving phlegm group (Codonopsis Radix, Atractylodis Macrocephalae Rhizoma, Poria, and Citri Reticulatae Pericarpium) targeted effective target genes such as ALDH7A1 and ACOX1 through 115 chemical components, regulated the AMPK and sphingolipid signaling pathways, significantly reduced the levels of diacylglycerol (DAG) and cholesterol esters, and effectively corrected lipid metabolism disorders. The activating blood circulation and dredging collaterals group (Angelicae Sinensis Radix, Chuanxiong Rhizoma, Paeoniae Radix Rubra, Achyranthis Bidentatae Radix, and Cinnamomi Ramulus) exerts effects through 197 chemical components by intervening in the chemokine and NOD-like receptor pathways, inhibiting the formation of neutrophil extracellular traps (NETs), downregulating inflammatory factor expression, and promoting vascular function repair. The tonifying the kidney and strengthening bones group (Rehmanniae Radix Praeparata and Cervi Cornu) regulated the PI3K/Akt and Ras/MAPK signaling pathways, inhibited osteoclast differentiation genes CTSK and MMP9, and facilitated the reconstruction of bone homeostasis. Transcriptomic and lipid metabolomic analyses were performed on clinical blood samples collected before and after treatment with Jianpi Huogu Formula. Multi-omics integration revealed that the three efficacy groups synergistically constructed a multidimensional network involving "lipid metabolism-immunity-bone homeostasis". A total of 594 differentially expressed effector genes (367 downregulated and 227 upregulated) were identified via clinical transcriptomics, and 179 differential lipid metabolites (mainly triglycerides and DAG) associated with the formula's efficacy were identified via lipid metabolomics. Together with 2 657 disease/syndrome-related genes, a "disease-syndrome-symptom-formula" association network was constructed. Topological eigenvalue analysis and functional mining indicated that the core network targets of Jianpi Huogu Formula in intervening SONFH mainly regulated signaling pathways such as osteoclast differentiation, apoptosis, Ras, MAPK, PI3K/Akt, and p53, thereby inhibiting osteoclast activity, promoting osteoblast proliferation, balancing bone resorption and formation, and improving the bone marrow microenvironment. This study systematically reveals the scientific basis of Jianpi Huogu Formula in intervening in the pathological process of SONFH through the synergistic action of "lipid metabolism reprogramming-transcriptional regulatory network" from three key dimensions, i. e., lipid metabolism, inflammation, and bone remodeling. It fully demonstrates the holistic advantages of traditional Chinese medicine (TCM) formulas in multi-component, multi-target, and multi-pathway coordinated regulation, and provides an innovative perspective and data support for elucidating the mechanism of TCM in the prevention and treatment of SONFH.

, 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=1276976067080491963, articleId=1276976066308740022, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=整合脂质代谢重编程与转录调控网络解析健脾活骨方治疗激素性股骨头坏死的功效科学内涵, 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=

综合运用临床转录组学、脂质代谢组学与生物分子网络挖掘技术，系统解析健脾活骨方治疗激素性股骨头坏死（SONFH）痰瘀阻络证的功效科学内涵。研究发现，健脾化痰组（党参、白术、茯苓、陈皮）通过115种化学成分靶向ALDH7A1、ACOX1等效应靶标基因，调控AMPK、鞘脂信号通路，显著降低甘油二酯（DAG）、胆固醇酯水平，有效纠正脂代谢紊乱；活血通络组（当归、川芎、赤芍、牛膝、桂枝）凭借197种化学成分干预趋化因子、NOD样受体通路，抑制中性粒细胞诱捕网形成，下调炎性因子表达，促进血管功能修复；补肾强骨组（熟地黄、鹿角）则通过调控PI3K/Akt、Ras/MAPK信号通路，抑制破骨分化基因CTSK和MMP9，推动骨稳态重建。进一步对健脾活骨方治疗SONFH前后的临床血样进行转录组学和脂质代谢组学检测，经多组学整合分析，揭示该方3个功效组协同构建起“脂代谢-免疫-骨稳态”多维作用网络。临床转录组筛选出594个方药干预前后差异表达的效应靶标基因（367个下调、227个上调），临床脂质代谢组鉴定出179个与方药疗效相关的差异脂质代谢物（以甘油三酯和DAG为主），结合2 657个病证基因构建“病-证-症-方”关联网络。通过拓扑特征值计算与功能挖掘显示，健脾活骨方干预SONFH的核心网络靶标主要通过调节破骨细胞分化、细胞凋亡、Ras、MAPK、PI3K/Akt和p53等信号通路，实现抑制破骨细胞活性、促进成骨细胞增殖、平衡骨吸收与骨形成过程、改善骨髓微环境的作用。该研究系统揭示了健脾活骨方通过“脂质代谢重编程-转录调控网络”协同作用，从脂代谢、炎症、骨重塑3个关键维度干预SONFH病理进程的功效科学内涵，充分体现了中医药复方多成分、多靶点、多通路协同调节的整体优势，为阐释中医药防治SONFH的作用机制提供了创新视角与数据支撑。

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