Article(id=1276976089993970140, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250919.401, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1755360000000, receivedDateStr=2025-08-17, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384424923, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384424923, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384424923, creator=13701087609, updateTime=1782384424923, 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=349, endPage=360, ext={EN=ArticleExt(id=1276976090195296734, articleId=1276976089993970140, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Mechanism of Jianpi Huogu Formula in promoting angiogenesis-osteogenesis coupling to treat steroid-induced osteonecrosis of femoral head in rats via VEGF-Notch-Noggin signaling pathway, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study aimed to observe the promoting effect of Jianpi Huogu Formula (JPHGF) on angiogenesis-osteogenesis coupling in rats with steroid-induced osteonecrosis of the femoral head (SONFH), and to explore its mechanism of action through the vascular endothelial growth factor (VEGF) -Notch-Noggin signaling pathway. A total of 120 Sprague-Dawley rats were randomly divided into a normal group, a model group, low-, medium-, and high-dose JPHGF groups (2.5, 5, and 10 g·kg^-1), and a Jiangusheng Pills group (1.53 g·kg^-1). Except for the normal group, all rats were injected with lipopolysaccharide (20 μg·kg^-1) via the tail vein once daily on days 1 and 2, followed by intramuscular injection of methylprednisolone sodium succinate (40 mg·kg^-1, gluteal muscle) once daily from days 3 to 5. The normal group received an equivalent volume of normal saline. Four weeks after model establishment, the rats were administered the corresponding drugs by gavage. The therapeutic effects of JPHGF on SONFH rats were evaluated by measuring mechanical pain threshold, cold pain sensitivity, hemorheological parameters, four coagulation indices, and by pathological and imaging analyses of the femoral head. The microvascular distribution of the femoral head was observed by ink perfusion and Microfil angiography. Immunofluorescence was used to detect the expression of platelet endothelial cell adhesion molecule-1 (CD31), endothelial mucin (Emcn), and the osteoblast-specific transcription factor Osterix, as well as the co-expression of CD31 and Noggin proteins in the femoral head. Immunohistochemistry was employed to detect the expression of type Ⅰ collagen (collagen Ⅰ) and Notch-1 proteins, while Western blot was used to measure the expression levels of VEGF and Noggin proteins in the femoral head. The results showed that JPHGF significantly increased the mechanical pain threshold and reduced the number of foot lifts in response to cold stimulation in SONFH rats. It markedly increased trabecular bone area, reduced the number of adipocytes and the percentage of empty lacunae, improved imaging manifestations of femoral head necrosis, and increased the vascular area in ink perfusion and the vessel volume in Microfil perfusion within the medullary cavity of the femoral head. JPHGF also improved hemorheological parameters and coagulation function, upregulated the expression of CD31, Emcn, and Osterix proteins, enhanced the co-expression of CD31 and Noggin proteins, and promoted the expression of collagen Ⅰ, Notch-1, VEGF, and Noggin proteins. These findings indicate that JPHGF promotes angiogenesis-osteogenesis coupling by activating the VEGF-Notch-Noggin signaling pathway, thereby effectively treating SONFH in rats. This study elucidates the pharmacological connotation of JPHGF from the perspective of "angiogenesis-osteogenesis coupling" and provides an experimental basis for its clinical application.

, authors=null, authorsList=Qian-qian YAN, Qun LI, Jia-lin WANG, Qing-yu ZHAO, Xiao-xuan LI, Chu-pei ZHENG, Wei-heng CHEN, Na LIN, Chun-fang LIU, authorCompany=null, correspAuthors=Na LIN, Chun-fang LIU, 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=1276976090539229664, articleId=1276976089993970140, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于VEGF-Notch-Noggin信号通路探索健脾活骨方促进成血管-成骨耦联治疗大鼠激素性股骨头坏死的作用机制, 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=

观察健脾活骨方（JPHGF）对大鼠激素性股骨头坏死（SONFH）成血管-成骨耦联的促进作用，并从血管内皮生长因子（VEGF） -Notch-Noggin信号通路探索其作用机制。将120只SD大鼠随机分为正常组，模型组，健脾活骨方低、中、高剂量（2.5、5、10 g·kg^-1）组和健骨生丸（1.53 g·kg^-1）组。除正常组外，每组第1、2天尾静脉注射20 μg·kg^-1脂多糖，每天1次；第3～5天均臀部肌肉注射40 mg·kg^-1甲泼尼龙琥珀酸钠，每天1次；同时正常组给予等体积生理盐水。造模4周后灌胃给药。通过检测机械痛、冷痛敏、血液流变学指标、凝血四项指标及股骨头病理和影像学分析评价JPHGF对SONFH大鼠的治疗作用；采用墨汁灌注和微血管造影灌注观察大鼠股骨头微血管分布情况；采用免疫荧光法检测大鼠股骨头血小板内皮细胞黏附分子-1（CD31）、内皮黏蛋白（Emcn）、成骨细胞特异性转录因子（Osterix）的表达情况及CD31、Noggin蛋白的共表达情况；采用免疫组化法检测大鼠股骨头Ⅰ型胶原蛋白（collagen Ⅰ）和Notch-1蛋白的表达；采用蛋白免疫印迹法检测大鼠股骨头VEGF和Noggin蛋白的表达。结果显示，JPHGF可显著升高SONFH大鼠机械痛阈值和减少冷痛敏反应抬脚次数，显著增加股骨头的骨小梁面积，降低脂肪细胞数、空骨陷窝率，改善股骨头影像学坏死情况，增加股骨头髓腔内墨汁灌注血管面积和Microfil灌注血管体积；改善血液流变和凝血功能，增加股骨头内CD31、Emcn、Osterix蛋白的表达以及CD31与Noggin蛋白共表达水平，同时促进collagen Ⅰ、Notch-1、VEGF、Noggin蛋白的表达。上述结果表明，JPHGF通过激活VEGF-Notch-Noggin信号通路促进成血管-成骨耦联，有效治疗大鼠SONFH，从“成血管-成骨耦联”角度阐述JPHGF功效内涵，为其临床应用提供实验依据。

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严倩倩，硕士研究生，E-mail: anqingyqq@126.com

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严倩倩，硕士研究生，E-mail: anqingyqq@126.com

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