To investigate changes in the gene expression profile and identify key inflammatory genes and signaling pathways involved in baicalin(BA)intervention against Listeria monocytogenes(LM)infection in murine macrophages, cells were divided into three groups:Control, LM-infected(LM), and BA-treated plus LM-infected(LM+BA). Following treatment, transcriptome sequencing(RNA-seq)was performed. Differentially expressed genes(DEGs)were screened and subjected to protein-protein interaction(PPI)analysis, Gene Ontology(GO)enrichment, and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis. Key findings were validated using reverse transcription-quantitative polymerase chain reaction(RT-qPCR). The results revealed 744 DEGs by comparing the LM group vs. the control group and the LM+BA group vs. the LM group. PPI analysis identified 82 core DEGs. These DEGs were primarily enriched in six inflammatory signaling pathways. RT-qPCR validation confirmed that the mRNA expression trends were consistent with the RNA-seq data. Therefore, we established BAs regulatory targets within LM-triggered inflammatory pathways, advancing our understanding of its anti-inflammatory properties and proposing new avenues for listeriosis control.- 引用格式:冯忠居,于明威,张聪,等.冲刷场地地震波形对大直径变截面单桩时程响应的影响[J].河北大学学报(自然科学版),2026,46(4):337-348.引用格式:张恩华,张宗昊,陈静,等.黄芩苷对LM感染的巨噬细胞炎性通路的影响[J].河北大学学报(自然科学版),2026,46(4):383-393.DOI:10.3969/j.issn.1000-1565.2026.04.006黄芩苷对LM感染的巨噬细胞炎性通路的影响张恩华1,2,张宗昊1,陈静1,赵子昂1,魏熙1,高政1,李文艳1(1.河北大学 基础医学院,河北 保定 071000;2. 河北大学 生命科学学院,河北 保定 071002)摘 要:为探究黄芩苷(baicalin,BA)干预单核细胞增生李斯特菌(Listeria monocytogenes, LM)感染小鼠巨噬细胞后基因表达谱的变化及其涉及的炎症关键基因和信号通路,将巨噬细胞分为3组:对照组、LM组和LM+BA组.对细胞处理后进行转录组测序,筛选出差异表达基因进行蛋白质互作、GO和KEGG分析,并通过RT-qPCR验证.结果显示:交叉分析LM组和对照组、LM+BA组和LM组,获得744个差异表达基因.蛋白质互作分析获得82个核心差异基因,主要富集的炎性通路6条.RT-qPCR结果表明mRNA表达趋势与测序结果相一致.因此,本研究筛选出了BA可能干预的LM引起炎症的相关信号通路和差异表达基因,为BA的抗炎机制和李斯特菌病的防治提供新思路.关键词:单核细胞增生李斯特菌;黄芩苷;转录组;RAW264.7细胞;炎性通路中图分类号:R392.12 文献标志码:A 文章编号:1000-1565(2026)04-0383-11DOI:10.3969/j.issn.1000-1565.2026.04.006Effect of baicalin on the inflammatory pathway of macrophages in LM infectionZHANG Enhua1,2, ZHANG Zonghao1, CHEN Jing1, ZHAO Ziang1, WEI Xi1, GAO Zheng1, LI Wenyan1(1. Basic Medical College, Hebei University, Baoding 071000,China;2. College of Life Sciences, Hebei University, Baoding 071002, China)Abstract: To investigate changes in the gene expression profile and identify key inflammatory genes and signaling pathways involved in baicalin(BA)intervention against Listeria monocytogenes(LM)infection in murine macrophages, cells were divided into three groups:Control, LM-infected(LM), and BA-treated plus LM-infected(LM+BA). Following treatment, transcriptome sequencing(RNA-seq)was performed. Differentially expressed genes(DEGs)were screened and subjected to protein-protein interaction(PPI)analysis, Gene Ontology(GO)enrichment, and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis. Key findings were validated using reverse transcription-quantitative polymerase chain reaction(RT-qPCR). The results revealed 744 DEGs by comparing the LM group vs. the control group and the LM+BA group vs. the LM group. PPI analysis identified 82 core DEGs. These DEGs were primarily enriched in six inflammatory signaling pathways. RT-qPCR validation confirmed that the mRNA expression trends were consistent with the RNA-seq data. Therefore, we established BAs regulatory targets within LM-triggered inflammatory pathways, advancing our understanding of its anti-inflammatory properties and proposing new avenues for listeriosis control.- 收稿日期:2025-06-26;修回日期:2025-09-27 基金项目:河北大学创新训练计划项目(S202510075134;DC2026560);河北大学实验室开放项目(sy202567);河北省中医药管理局项目(2023136) 第一作者:张恩华(1998—),女,河北大学在读博士研究生,主要从事分子生物学研究.E-mail:ly2580233@163.com 通信作者:李文艳(1973—),女,河北大学副教授,博士,主要从事生殖生物学研究.E-mail:liwenyan358@163.com 第4期张恩华等:黄芩苷对LM感染的巨噬细胞炎性通路的影响河北大学学报(自然科学版) 第46卷
[1] Zhao Q, Hu P, Li Q Q, et al. Prevalence and transmission characteristics of Listeria species from ruminants in farm and slaughtering environments in China[J]. Emerg Microbes Infect, 2021, 10(1):356-364. DOI:10.1080/22221751.2021.1888658.
[2] Giralt-Zúñiga M, Redondo-Solano M, Moura A, et al. Genome-based characterization of Listeria monocytogenes, costa rica[J]. Emerg Infect Dis, 2023, 29(12):2566-2569.. DOI:10.3201/eid2912.230774.
[3] Mayer R L, Verbeke R, Asselman C, et al. Immunopeptidomics-based design of mRNA vaccine formulations against Listeria monocytogenes[J]. Nat Commun, 2022, 13:6075. DOI:10.1038/s41467-022-33721-y.
[4] Charlier C, Disson O, Lecuit M. Maternal-neonatal listeriosis[J]. Virulence, 2020, 11(1):391-397. DOI:10.1080/21505594.2020.1759287.
[5] Gattuso A, Cella E, Fillo S, et al. Phylogenetic and evolutionary genomic analysis of Listeria monocytogenes clinical strains in the framework of foodborne listeriosis risk assessment[J]. Front Microbiol, 2022, 13:816880. DOI:10.3389/fmicb.2022.816880.
[6] Koopmans M M, Brouwer M C, Vázquez-Boland J A, et al. Human listeriosis[J]. Clin Microbiol Rev, 2023, 36:e00060-e00019. DOI:10.1128/cmr.00060-19.
[7] Soria-Castro R, Alfaro-Doblado á R, Rodríguez-López G, et al. TLR2 regulates mast cell IL-6 and IL-13 production during Listeria monocytogenes infection[J]. Front Immunol, 2021, 12:650779. DOI:10.3389/fimmu.2021.650779.
[8] Tan J M J, Garner M E, Regeimbal J M, et al. Listeria exploits IFITM3 to suppress antibacterial activity in phagocytes[J]. Nat Commun, 2021, 12:4999. DOI:10.1038/s41467-021-24982-0.
[9] Schlech W F III. Epidemiology and clinical manifestations of Listeria monocytogenes infection[J]. Microbiol Spectr, 2019, 7(3):7.3.3. DOI:10.1128/microbiolspec.gpp3-0014-2018.
[10] Bookstaver P B, Bland C M, Griffin B, et al. A review of antibiotic use in pregnancy[J]. Pharmacotherapy, 2015, 35(11):1052-1062. DOI:10.1002/phar.1649.
[11] Rocha C E V, Silva M F, Guedes A C B, et al. Alginate-chitosan microcapsules improve vaccine potential of gamma-irradiated Listeria monocytogenes against listeriosis in murine model[J]. Int J Biol Macromol, 2021, 176:567-577. DOI:10.1016/j.ijbiomac.2021.02.056.
[12] Kew O, Morris-Glasgow V, Landaverde M, et al. Outbreak of poliomyelitis in Hispaniola associated with circulating type 1 vaccine-derived poliovirus[J]. Science, 2002, 296(5566):356-359. DOI:10.1126/science.1068284.
[13] Yan Y R, Zhang L, Lin Y N, et al. Chronic intermittent hypoxia-induced mitochondrial dysfunction mediates endothelial injury via the TXNIP/NLRP3/IL-1β signaling pathway[J]. Free Radic Biol Med, 2021, 165:401-410. DOI:10.1016/j.freeradbiomed.2021.01.053.
[14] Huang J H, Zhang X Y, Yang X P, et al. Baicalin exerts neuroprotective actions by regulating the Nrf2-NLRP3 axis in toxin-induced models of Parkinson’s disease[J]. Chem Biol Interact, 2024, 387:110820. DOI:10.1016/j.cbi.2023.110820.
[15] Wei X H, Zhang B P, Wei F Y, et al. Gegen Qinlian pills alleviate carrageenan-induced thrombosis in mice model by regulating the HMGB1/NF-κB/NLRP3 signaling[J]. Phytomedicine, 2022, 100:154083. DOI:10.1016/j.phymed.2022.154083.
[16] 钱秋然,王杰平,张艳荣,等.基于PI3K/Akt信号通路探讨黄芩苷调节复发性流产小鼠子宫母胎界面免疫状态的影响[J].中医药信息, 2022, 39(8):8-13. DOI:10.19656/j.cnki.1002-2406.20220802.
[17] Wu Y L, Wang F, Fan L H, et al. Baicalin alleviates atherosclerosis by relieving oxidative stress and inflammatory responses via inactivating the NF-κB and p38 MAPK signaling pathways[J]. Biomed Pharmacother, 2018, 97:1673-1679. DOI:10.1016/j.biopha.2017.12.024.
[18] Fu Y J, Xu B, Huang S W, et al. Baicalin prevents LPS-induced activation of TLR4/NF-κB p65 pathway and inflammation in mice via inhibiting the expression of CD14[J]. Acta Pharmacol Sin, 2021, 42(1):88-96. DOI:10.1038/s41401-020-0411-9.
[19] 刘雯,张恩华,陈滢滢,等.黄芩苷对单增李斯特菌诱导巨噬细胞炎性小体激活的抑制作用[J].河北大学学报(自然科学版), 2024, 44(4):399-405. DOI: 10.3969/j.issn.1000-1565.2024.04.008.
[20] 魏滋鸿.黄芩提取物抗单增李斯特菌感染的作用的研究[D].长春:吉林大学, 2018.
[21] Karakaslar E O, Katiyar N, Hasham M, et al. Transcriptional activation of Jun and Fos members of the AP-1 complex is a conserved signature of immune aging that contributes to inflammaging[J]. Aging Cell, 2023, 22(4):e13792. DOI:10.1111/acel.13792.
[22] Song D D, Lian Y, Zhang L. The potential of activator protein 1(AP-1)in cancer targeted therapy[J]. Front Immunol, 2023, 14:1224892. DOI:10.3389/fimmu.2023.1224892.
[23] Zhang C, Yu M M, Hepperla A J, et al. Von Hippel Lindau tumor suppressor controls m6A-dependent gene expression in renal tumorigenesis[J]. J Clin Investig, 2024, 134(8):e175703. DOI:10.1172/jci175703.
[24] Esen I, Sandovici M, Heeringa P, et al. Impaired IL-6-induced JAK-STAT signaling in CD4+ T cells associates with longer treatment duration in giant cell arteritis[J]. J Autoimmun, 2024, 146:103215. DOI:10.1016/j.jaut.2024.103215.
[25] Cheng D M, Lian W X, Wang T, et al. The interplay of Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils proactively mediates silica-induced pulmonary fibrosis[J]. J Hazard Mater, 2024, 467:133713. DOI:10.1016/j.jhazmat.2024.133713.
[26] Chang T T, Lin L Y, Chen C, et al. CCL4 contributes to aging related angiogenic insufficiency through activating oxidative stress and endothelial inflammation[J]. Angiogenesis, 2024, 27(3):475-499. DOI:10.1007/s10456-024-09922-y.
[27] Chen R, Yang X, Liu Q, et al. Research progresses on the effects of CCL4 on immune escape in tumor microenvironment[J]. Chin J Lung Cancer, 2024, 27(8):613-621. doi:10.3779/j.issn.1009-3419.2024.106.23.
[28] Tang J T, Gao K C, Zhang Y, et al. ERK/STAT3 activation through CCL17/CCR4 axis-mediated type 2 cytokine-involved signaling pathways in Th2 cells regulates cutaneous drug reactions[J]. Int Immunopharmacol, 2024, 130:111712. DOI:10.1016/j.intimp.2024.111712.
[29] Yue S Y, Niu D, Ma W M, et al. The CXCL10/CXCR3 axis regulates Th1 cell differentiation and migration in experimental autoimmune prostatitis through the PI3K/AKT pathway[J]. Andrology, 2024, 12(6):1408-1418. DOI:10.1111/andr.13571.
[30] Rosain J, Neehus A L, Manry J, et al. Human IRF1 governs macrophagic IFN-γ immunity to mycobacteria[J]. Cell, 2023, 186(3):621-645.e33. DOI:10.1016/j.cell.2022.12.038.
[31] Ahn B Y, Zhang Y, Wei S B, et al. Prmt7 regulates the JAK/STAT/Socs3 signaling pathway in postmenopausal cardiomyopathy[J]. Exp Mol Med, 2024, 56(3):711-720. DOI:10.1038/s12276-024-01193-3.
[32] Yan D M, Li G N, Yuan Y, et al. SOCS3 inhibiting JAK-STAT pathway enhances oncolytic adenovirus efficacy by potentiating viral replication and T-cell activation[J]. Cancer Gene Ther, 2024, 31(3):397-409. DOI:10.1038/s41417-023-00710-2.
[33] Zanders L, Kny M, Hahn A, et al. Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting[J]. J Cachexia Sarcopenia Muscle, 2022, 13(1):713-727. DOI:10.1002/jcsm.12867. (