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Article(id=1276976067223093565, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251011.701, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1751904000000, receivedDateStr=2025-07-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384419493, onlineDateStr=2026-06-25, pubDate=1767196800000, pubDateStr=2026-01-01, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384419493, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384419493, creator=13701087609, updateTime=1782384419493, updator=13701087609, issue=Issue{id=1276975955985961244, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='1', pageStart='1', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1767196800000', pubDateStr='2026-01-01', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1782384392973, creator='13701087609', updateTime=1782384484405, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976339546673871, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976339546673872, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=133, endPage=142, ext={EN=ArticleExt(id=1276976067399254335, articleId=1276976067223093565, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Mechanisms of Tanyu Tongzhi Optimization Decoction against hyperlipidemia based on transcriptomics and proteomics, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study established a hyperlipidemia model by feeding Sprague-Dawley rats a high-fat diet for 8 weeks. The rats were randomly assigned to the following groups: model group, atorvastatin calcium group (4.8 mg·kg-1), low-, medium-, and high-dose Tanyu Tongzhi Optimization Decoction (TYTZD) groups (3.6, 7.2, and 14.4 g·kg-1), and a normal diet control group. After 4 weeks of continuous administration, hematoxylin-eosin (HE) and oil red O staining were used to observe liver pathological changes and lipid infiltration. Automatic biochemical analyzer were performed to assess blood lipid profiles, coagulation function, and liver function. Transcriptomic and proteomic analyses were employed to identify differentially expressed genes (DEGs) and proteins (DEPs), followed by enrichment analysis. The MCODE algorithm was applied to classify DEGs and DEPs into modules, and network separation index (SAB) was calculated to assess module separation, enabling construction of a gene-protein co-expression network for core target screening. The diagnostic accuracy of core targets was evaluated by area under the receiver operating characteristic (ROC) curve (AUC), and ELISA was used to measure core target expression. Western blot detected the expression of core pathway-related proteins in liver tissue. Results demonstrated that TYTZD significantly improved dyslipidemia, coagulation dysfunction, liver injury, hepatic pathology, and lipid infiltration in hyperlipidemic rats. Transcriptomic analysis identified 571 DEGs significantly reversed by TYTZD, mainly enriched in inflammatory signaling pathways such as Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB). Proteomic analysis identified 102 reversed DEPs, mainly involved in cholesterol metabolism pathways. Integrated analysis identified core targets including TLR4, tumor necrosis factor-α (TNF-α), integrin subunit alpha M (ITGAM), Toll-like receptor 2 (TLR2), matrix metalloproteinase 9 (MMP9), interleukin-1β (IL-1β), apolipoprotein E (APOE), and apolipoprotein C2 (APOC2), all with AUC values greater than 0.70. ELISA showed that TYTZD intervention significantly downregulated MMP9, TNF-α, IL-1β, TLR2, ITGAM, and TLR4, and upregulated APOC2 and APOE. Western blot indicated that TYTZD reduced TLR4, p-NF-κB, and IL-1β protein expression in liver tissue. In conclusion, TYTZD may exert anti-hyperlipidemic effects through regulation of core targets such as ITGAM, TLR4, and APOC2, and by modulating the TLR4/NF-κB signaling pathway to intervene in inflammatory responses and cholesterol metabolism, thereby achieving multi-target, multi-pathway therapeutic effects against hyperlipidemia.

, authors=null, authorsList=Ying YANG, Xiang LI, Dan-li TANG, Bing LI, Si-jia WU, Wen-jing ZONG, Hua-min ZHANG, authorCompany=null, correspAuthors=Wen-jing ZONG, Hua-min 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=1276976067608969537, articleId=1276976067223093565, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于转录组学和蛋白组学探讨痰瘀同治优化方抗高脂血症作用机制, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

该研究采用高脂饲料喂养SD大鼠8周建立高脂血症模型，随机分为模型组，阿托伐他汀钙组（4.8 mg·kg-1），痰瘀同治优化方低、中、高剂量组（3.6、7.2、14.4 g·kg-1）及对照组。连续给药4周后，苏木精-伊红（HE）和油红O染色观察大鼠肝组织病理变化以及脂肪浸润情况；全自动生化仪检测血脂、凝血功能以及肝功能；运用转录组学和蛋白质组学技术筛选差异表达基因（DEGs）与差异表达蛋白（DEPs），进行富集分析；采用MCODE算法划分DEGs和DEPs模块，结合网络分离指数（SAB）计算模块分离度，构建基因-蛋白共表达网络以筛选核心靶点，并利用受试者工作特征（ROC）曲线下面积（AUC）评价核心靶点的诊断准确性，ELISA检测核心靶点表达水平，Western blot检测大鼠肝脏核心通路相关蛋白表达水平。结果显示，痰瘀同治优化方能够显著改善高脂血症大鼠的血脂紊乱、凝血功能异常、肝功能损伤以及肝脏病理学变化和脂肪浸润。转录组分析鉴定出571个经该方干预后显著回调的DEGs，主要富集于Toll样受体4（TLR4）/转录因子-κB（NF-κB）等炎症信号通路；蛋白质组学分析则筛选出102个回调DEPs，其富集通路主要涉及胆固醇代谢。通过整合分析，筛选出核心靶点为TLR4、肿瘤坏死因子-α（TNF-α）、整合素αM（ITGAM）、Toll样受体2（TLR2）、基质金属蛋白酶9（MMP9）、白细胞介素-1β（IL-1β）、载脂蛋白E（APOE）和载脂蛋白C2（APOC2），且核心靶点AUC值均大于0.70。ELISA结果显示，痰瘀同治优化方干预显著降低MMP9、TNF-α、IL-1β、TLR2、ITGAM、TLR4表达水平，升高APOC2、APOE水平；Western blot结果显示痰瘀同治优化方可降低肝脏组织TLR4、p-NF-κB、IL-1β蛋白表达水平。综上，痰瘀同治优化方可能通过调控ITGAM、TLR4、APOC2等核心靶点及调控TLR4/NF-κB信号通路干预炎症反应及胆固醇代谢，从而发挥其多靶点、多途径抗高脂血症的作用。

, authors=

杨莹，博士研究生，主要从事中医药防治心血管病基础研究，E-mail:

, authorsList=杨莹, 李想, 唐丹丽, 李兵, 吴斯佳, 宗文静, 张华敏, authorCompany=null, correspAuthors=宗文静, 张华敏, authorNote=null, correspAuthorsNote=

*

宗文静，博士，讲师，主要从事中医药防治心血管病基础研究，E-mail: ；

*

张华敏，博士，研究员，主要从事中医药防治心血管病基础研究，E-mail:
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杨莹，博士研究生，主要从事中医药防治心血管病基础研究，E-mail:

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基于转录组学和蛋白组学探讨痰瘀同治优化方抗高脂血症作用机制
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杨莹 1 , 李想 1 , 唐丹丽 2 , 李兵 3 , 吴斯佳 3 , 宗文静 1, * , 张华敏 1, *
中国中药杂志 | 药理 2026,51(1): 133-142
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中国中药杂志 |药理 2026 , 51 (1) : 133 -142
基于转录组学和蛋白组学探讨痰瘀同治优化方抗高脂血症作用机制
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杨莹1 , 李想1, 唐丹丽2, 李兵3, 吴斯佳3, 宗文静1, * , 张华敏1, *
作者信息
  • 1．中国中医科学院 中医基础理论研究所，北京 100700
  • 2．中国中医科学院 医学实验中心，北京 100700
  • 3．中国中医科学院 中药研究所，北京 100700
通讯作者:

*

宗文静，博士，讲师，主要从事中医药防治心血管病基础研究，E-mail: ；

*

张华敏，博士，研究员，主要从事中医药防治心血管病基础研究，E-mail:
Mechanisms of Tanyu Tongzhi Optimization Decoction against hyperlipidemia based on transcriptomics and proteomics
Ying YANG1 , Xiang LI1, Dan-li TANG2, Bing LI3, Si-jia WU3, Wen-jing ZONG1, * , Hua-min ZHANG1, *
Affiliations
  • 1.Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China
  • 2.Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing 100700, China
  • 3.Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China
出版时间: 2026-01-01 doi: 10.19540/j.cnki.cjcmm.20251011.701
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该研究采用高脂饲料喂养SD大鼠8周建立高脂血症模型，随机分为模型组，阿托伐他汀钙组（4.8 mg·kg-1），痰瘀同治优化方低、中、高剂量组（3.6、7.2、14.4 g·kg-1）及对照组。连续给药4周后，苏木精-伊红（HE）和油红O染色观察大鼠肝组织病理变化以及脂肪浸润情况；全自动生化仪检测血脂、凝血功能以及肝功能；运用转录组学和蛋白质组学技术筛选差异表达基因（DEGs）与差异表达蛋白（DEPs），进行富集分析；采用MCODE算法划分DEGs和DEPs模块，结合网络分离指数（SAB）计算模块分离度，构建基因-蛋白共表达网络以筛选核心靶点，并利用受试者工作特征（ROC）曲线下面积（AUC）评价核心靶点的诊断准确性，ELISA检测核心靶点表达水平，Western blot检测大鼠肝脏核心通路相关蛋白表达水平。结果显示，痰瘀同治优化方能够显著改善高脂血症大鼠的血脂紊乱、凝血功能异常、肝功能损伤以及肝脏病理学变化和脂肪浸润。转录组分析鉴定出571个经该方干预后显著回调的DEGs，主要富集于Toll样受体4（TLR4）/转录因子-κB（NF-κB）等炎症信号通路；蛋白质组学分析则筛选出102个回调DEPs，其富集通路主要涉及胆固醇代谢。通过整合分析，筛选出核心靶点为TLR4、肿瘤坏死因子-α（TNF-α）、整合素αM（ITGAM）、Toll样受体2（TLR2）、基质金属蛋白酶9（MMP9）、白细胞介素-1β（IL-1β）、载脂蛋白E（APOE）和载脂蛋白C2（APOC2），且核心靶点AUC值均大于0.70。ELISA结果显示，痰瘀同治优化方干预显著降低MMP9、TNF-α、IL-1β、TLR2、ITGAM、TLR4表达水平，升高APOC2、APOE水平；Western blot结果显示痰瘀同治优化方可降低肝脏组织TLR4、p-NF-κB、IL-1β蛋白表达水平。综上，痰瘀同治优化方可能通过调控ITGAM、TLR4、APOC2等核心靶点及调控TLR4/NF-κB信号通路干预炎症反应及胆固醇代谢，从而发挥其多靶点、多途径抗高脂血症的作用。

高脂血症  /  瓜蒌薤白半夏汤  /  痰瘀同治优化方  /  转录组学  /  蛋白组学  /  网络分离指数

This study established a hyperlipidemia model by feeding Sprague-Dawley rats a high-fat diet for 8 weeks. The rats were randomly assigned to the following groups: model group, atorvastatin calcium group (4.8 mg·kg-1), low-, medium-, and high-dose Tanyu Tongzhi Optimization Decoction (TYTZD) groups (3.6, 7.2, and 14.4 g·kg-1), and a normal diet control group. After 4 weeks of continuous administration, hematoxylin-eosin (HE) and oil red O staining were used to observe liver pathological changes and lipid infiltration. Automatic biochemical analyzer were performed to assess blood lipid profiles, coagulation function, and liver function. Transcriptomic and proteomic analyses were employed to identify differentially expressed genes (DEGs) and proteins (DEPs), followed by enrichment analysis. The MCODE algorithm was applied to classify DEGs and DEPs into modules, and network separation index (SAB) was calculated to assess module separation, enabling construction of a gene-protein co-expression network for core target screening. The diagnostic accuracy of core targets was evaluated by area under the receiver operating characteristic (ROC) curve (AUC), and ELISA was used to measure core target expression. Western blot detected the expression of core pathway-related proteins in liver tissue. Results demonstrated that TYTZD significantly improved dyslipidemia, coagulation dysfunction, liver injury, hepatic pathology, and lipid infiltration in hyperlipidemic rats. Transcriptomic analysis identified 571 DEGs significantly reversed by TYTZD, mainly enriched in inflammatory signaling pathways such as Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB). Proteomic analysis identified 102 reversed DEPs, mainly involved in cholesterol metabolism pathways. Integrated analysis identified core targets including TLR4, tumor necrosis factor-α (TNF-α), integrin subunit alpha M (ITGAM), Toll-like receptor 2 (TLR2), matrix metalloproteinase 9 (MMP9), interleukin-1β (IL-1β), apolipoprotein E (APOE), and apolipoprotein C2 (APOC2), all with AUC values greater than 0.70. ELISA showed that TYTZD intervention significantly downregulated MMP9, TNF-α, IL-1β, TLR2, ITGAM, and TLR4, and upregulated APOC2 and APOE. Western blot indicated that TYTZD reduced TLR4, p-NF-κB, and IL-1β protein expression in liver tissue. In conclusion, TYTZD may exert anti-hyperlipidemic effects through regulation of core targets such as ITGAM, TLR4, and APOC2, and by modulating the TLR4/NF-κB signaling pathway to intervene in inflammatory responses and cholesterol metabolism, thereby achieving multi-target, multi-pathway therapeutic effects against hyperlipidemia.

hyperlipidemia  /  Gualou Xiebai Banxia Decoction  /  Tanyu Tongzhi Optimization Decoction  /  transcriptomics  /  proteomics  /  network separation index
杨莹, 李想, 唐丹丽, 李兵, 吴斯佳, 宗文静, 张华敏. 基于转录组学和蛋白组学探讨痰瘀同治优化方抗高脂血症作用机制. 中国中药杂志, 2026 , 51 (1) : 133 -142 . DOI: 10.19540/j.cnki.cjcmm.20251011.701
Ying YANG, Xiang LI, Dan-li TANG, Bing LI, Si-jia WU, Wen-jing ZONG, Hua-min ZHANG. Mechanisms of Tanyu Tongzhi Optimization Decoction against hyperlipidemia based on transcriptomics and proteomics[J]. Chinese Journal of Traditional Chinese Medicine, 2026 , 51 (1) : 133 -142 . DOI: 10.19540/j.cnki.cjcmm.20251011.701
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  • 中国中医科学院科技创新工程项目中医理论传承与创新专项(KYG-202404)
  • 国家自然科学基金项目(82374182)
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doi: 10.19540/j.cnki.cjcmm.20251011.701
  • 接收时间：2025-07-08
  • 首发时间：2026-06-25
  • 出版时间：2026-01-01
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  • 收稿日期：2025-07-08
基金
中国中医科学院科技创新工程项目中医理论传承与创新专项(KYG-202404)
国家自然科学基金项目(82374182)
作者信息
    1．中国中医科学院 中医基础理论研究所，北京 100700
    2．中国中医科学院 医学实验中心，北京 100700
    3．中国中医科学院 中药研究所，北京 100700

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*

宗文静，博士，讲师，主要从事中医药防治心血管病基础研究，E-mail: ；

*

张华敏，博士，研究员，主要从事中医药防治心血管病基础研究，E-mail:
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https://castjournals.cast.org.cn/joweb/zgzyzz/CN/10.19540/j.cnki.cjcmm.20251011.701
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
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