芪红胶囊对慢性心力衰竭大鼠胸主动脉基因表达的调控机制*

作者：翟雪芹，高 玉，王晓峰

单位：新疆医科大学第四临床医学院，新疆 乌鲁木齐 830000

引用：引用：翟雪芹，高玉，王晓峰.芪红胶囊对慢性心力衰竭大鼠胸主动脉基因表达的调控机制[J].中医药导报,2026,32(1):64-70.

DOI：10.13862/j.cn43-1446/r.2026.01.010

PDF： 下载PDF

摘要：

目的：探讨芪红胶囊对慢性心力衰竭（CHF）大鼠主动脉基因表达模式的调控作用及其机制。方法：将18只大鼠随机分为假手术组、模型组和芪红胶囊干预组，每组6只。模型组和芪红胶囊干预组通过胸主动脉缩窄术构建CHF大鼠模型，芪红胶囊干预组给予芪红胶囊（0.648 g/kg）灌胃，假手术组、模型组给予等体积生理盐水（10 mL/kg）灌胃，连续干预28 d。末次给药8 h后，留取胸主动脉组织，提取总RNA进行转录组测序（RNA-seq）并获取数据。利用生物信息学分析识别差异表达基因（DEGs），并对其进行基因本体（GO）功能富集和京都基因与基因组百科全书（KEGG）通路富集，探讨潜在的功能机制。利用MSigDB数据库进行基因集变异分析，进一步构建蛋白质互作（PPI）网络。整合CHF相关基因及芪红胶囊活性成分，构建“芪红胶囊-中药活性成分-靶点-CHF”互作网络。结果：DEGs显著富集于B细胞受体信号通路、B细胞分化、T细胞增殖正调控及红细胞稳态通路，提示芪红胶囊可能通过免疫调控改善CHF。神经嵴细胞迁移、自噬的正向调控及雌二醇反应基因集在治疗中发挥关键作用。靶点基因（Ryr1、Cacna1d、Gpx1、Txnip、Ptgs2、Dusp1、Erbb4、Rock1、Lrrk2）与上述生物学过程密切相关，Gpr35和Fgg是芪红胶囊调控CHF的关键靶点。结论：芪红胶囊可通过多靶点、多通路（如炎症反应、免疫功能、自噬、氧化应激等）干预CHF进展，其核心成分（醇类、酸类、氨基酸衍生物等）可通过Gpr35和Fgg等关键靶点发挥治疗作用。

关键词：慢性心力衰竭；芪红胶囊；转录组测序；差异表达基因；大鼠

Abstract：

Objective: To investigate the regulatory effect and mechanism of Qihong capsule on the gene expression profile in the aorta of rats with chronic heart failure (CHF). Methods: A total of 18 rats were randomly divided into the sham-operated group, model group, and Qihong capsule intervention group, with 6 rats in each group. The CHF model was established by thoracic aortic constriction in the model group and Qihong capsule intervention group. The Qihong capsule intervention group was administered Qihong capsule (0.648 g/kg) by gavage, while the sham-operated group and model group received an equal volume of normal saline(10 mL/kg) for 28 consecutive days. Eight hours after the last administration, thoracic aortic tissues were collected, and total RNA was extracted for transcriptome sequencing (RNA-seq). Differentially expressed genes (DEGs) were identified through bioinformatics analysis, followed by Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore potential functional mechanisms. Gene set variation analysis was performed using the MSigDB database, and a protein-protein interaction (PPI) network was constructed. An interaction network of "Qihong capsule-active components-targets-CHF" was built by integrating CHF-related genes and the active components of Qihong capsule. Results: DEGs were significantly enriched in pathways such as the B cell receptor signaling pathway, B cell differentiation, positive regulation of T cell proliferation, and erythrocyte homeostasis, suggesting that Qihong capsule may improve CHF through immunomodulation. Gene sets related to neural crest cell migration, positive regulation of autophagy, and cellular response to estradiol played key roles in the treatment. Target genes (Ryr1, Cacna1d, Gpx1, Txnip, Ptgs2, Dusp1, Erbb4, Rock1, Lrrk2) were closely associated with the aforementioned biological processes. and Gpr35 and Fgg were key targets through which Qihong capsule regulates CHF. Conclusion: Qihong capsule may intervene in the progression of CHF through multiple targets and pathways (inflammatory response, immune function, autophagy, oxidative stress, etc.). Its core components (alcohols, acids, amino acid derivatives, etc.) likely exert therapeutic effects by acting on key targets such as Gpr35 and Fgg.

Key words：chronic heart failure; Qihong capsule; transcriptome sequencing; differentially expressed genes; rat

发布时间：2026-01-30

点击量：0