Objective: To explore the mechanism of Mongolian medicine Sendeng-9 Decoction (Brucellosis Ⅱ) in the treatment of brucellosis by network pharmacology. Methods: The BATMAN-TCM database was used to analyze the active components and potential targets of Mongolian medicine Sendeng-9 decoction. Brucellosis-related targets were screened through Genecards, OMIM, and DisGeNET databases. The Venn diagram was constructed to obtain the intersection target of disease and the intersection target of Mongolian medicine Sendeng-9 decoction in the treatment of brucellosis. The network diagram of “drug-component-disease-target” relationship was drawn by Cytoscape software. The protein-protein interaction (PPI) network of ' active ingredient-disease ' common targets was constructed by STRING database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of key targets were performed using the David database. Results: There were 182 active components of Mongolian medicine Sendeng-9 Decoction, which acted on 1306 targets. There were 620 brucellosis targets and 152 drug-disease intersection targets. The main active ingredients of Mongolian medicine Sendeng-9 Decoction in the treatment of brucellosis were lauric acid, myristic acid, linoleic acid, jasmonone, lupinone, geranylacetone, oxysophocarpine, 3-nonen-2-one, etc. The core targets for the treatment of brucellosis were IL-6, IL-1β, INS, TNF, PTGS2, JUN, TP53, IGF1, CCL2, HIF1A. A total of 1064 GO entries were obtained, including 834 BP entries, 107 CC entries, and 123 MF entries. There were 162 KEGG signaling pathways, mainly focusing on HIF-1 signaling pathway, TNF signaling pathway, MAPK signaling pathway, FoxO signaling pathway, IL-17 signaling pathway and so on. Conclusion: Through the method of network pharmacology, this study preliminarily discusses the anti-inflammatory and disease-resistant pathogenic microorganisms of the effective components of Mongolian medicine Senden-9 decoction, which provides a theoretical basis for the treatment of brucellosis, and further study of the mechanism of action and clinical application of this prescription.
[1] Zheng RJ, Xie SS, Lu XB, et al. A systematic review and meta-analysis of epidemiology and clinical manifestations of human brucellosis in China[J]. Biomed Res Int, 2018, 2018: 5712920.
[2] Deng YM, Liu XY, Duan KF, et al. Research progress on brucellosis[J]. Curr Med Chem, 2019, 26(30): 5598-5608.
[3] Wang Y, Wang Y, Zhang LN, et al. An epidemiological study of brucellosis on mainland China during 2004-2018[J]. Transbound Emerg Dis, 2021, 68(4): 2353-2363.
[4] 毕圣贤, 别思羽, 张辉国, 等. 基于时空加权泊松回归模型的全国布鲁氏菌病分布特征与影响因素分析[J]. 中国卫生统计, 2022, 39(3): 405-408, 412.
[5] 樊晓玲, 樊永贞. 蒙医蒙药治疗布鲁杆菌病临床研究进展[J]. 疾病监测与控制, 2015, 9(2): 95-97.
[6] Jiao HW, Zhou ZX, Li BW, et al. The mechanism of facultative intracellular parasitism of Brucella[J]. Int J Mol Sci, 2021, 22(7): 3673.
[7] 巴雅尔图, 巴图吉日嘎啦. 名蒙医巴图吉日嘎啦教授学术思想及蒙医药治疗布鲁氏菌病临床研究[J]. 世界最新医学信息文摘, 2018, 18(94): 174, 181.
[8] 德胜, 宝喜春. 蒙药治疗重症布病优势分析[J]. 中国民族医药杂志, 2021, 27(5): 26-27, 55.
[9] 王梅, 王晓娟. HPLC法测定森登-9汤中栀子苷的含量[J]. 中国民族医药杂志, 2014, 20(1): 41-42.
[10] Nogales C, Mamdouh ZM, List M, et al. Network pharmacology: curing causal mechanisms instead of treating symptoms[J]. Trends Pharmacol Sci, 2022, 43(2): 136-150.
[11] 谭婉静, 张笑薇, 白泓, 等. 丁香油与月桂酸对金黄色葡萄球菌的协同抑制作用[J]. 现代食品科技, 2022, 38(2): 278-285, 265.
[12] Jin X, Zhou JC, Richey G, et al. Undecanoic acid, lauric acid, and N-tridecanoic acid inhibit Escherichia coli persistence and biofilm formation[J]. J Microbiol Biotechnol, 2021, 31(1): 130-136.
[13] Khan HU, Aamir K, Jusuf PR, et al. Lauric acid ameliorates lipopolysaccharide (LPS)-induced liver inflammation by mediating TLR4/MyD88 pathway in Sprague Dawley (SD) rats[J]. Life Sci, 2021, 265: 118750.
[14] Alonso-Castro AJ, Serrano-Vega R, Pérez Gutiérrez S, et al. Myristic acid reduces skin inflammation and nociception[J]. J Food Biochem, 2022, 46(1): e14013.
[15] Den Hartigh LJ. Conjugated linoleic acid effects on cancer, obesity, and atherosclerosis: a review of pre-clinical and human trials with current perspectives[J]. Nutrients, 2019, 11(2): 370.
[16] Watkins BA, Seifert MF. Conjugated linoleic acid and bone biology[J]. J Am Coll Nutr, 2000, 19(4): 478S-486S.
[17] Lin ZQ, Lin GY, He WW, et al. IL-6 and INF-γ levels in patients with brucellosis in severe epidemic region, Xinjiang, China[J]. Infect Dis Poverty, 2020, 9(1): 47.
[18] Raghu H, Lepus CM, Wang Q, et al. CCL2/CCR2, but not CCL5/CCR5, mediates monocyte recruitment, inflammation and cartilage destruction in osteoarthritis[J]. Ann Rheum Dis, 2017, 76(5): 914-922.
[19] Sierra-Filardi E, Nieto C, Domínguez-Soto A, et al. CCL2 shapes macrophage polarization by GM-CSF and M-CSF: identification of CCL2/CCR2-dependent gene expression profile[J]. J Immunol, 2014, 192(8): 3858-3867.
[20] Devraj G, Beerlage C, Brüne B, et al. Hypoxia and HIF-1 activation in bacterial infections[J]. Microbes Infect, 2017, 19(3): 144-156.
[21] Balamurugan K. HIF-1 at the crossroads of hypoxia, inflammation, and cancer[J]. Int J Cancer, 2016, 138(5): 1058-1066.
[22] Dehne N, Brüne B. HIF-1 in the inflammatory microenvironment[J]. Exp Cell Res, 2009, 315(11): 1791-1797.
[23] 杨梦思, 周娜, 王志钢, 等. 转录因子HIF-1α及其信号通路在疾病发生中的作用研究进展[J]. 生物技术通报, 2016, 32(8): 8-13.
[25] 杨亚军, 崔燎. FoxO/Wnt通路在氧化应激介导的骨质疏松中的调控机制[J]. 中国药理学通报, 2013, 29(1): 27-30.
[26] Lee Y, Kim YJ, Kim MH, et al. MAPK cascades in guard cell signal transduction[J]. Front Plant Sci, 2016, 7: 80.
[27] Yeung YT, Aziz F, Guerrero-Castilla A, et al. Signaling pathways in inflammation and anti-inflammatory therapies[J]. Curr Pharm Des, 2018, 24(14):1449-1484.
[28] Zhang YJ, Zhu TF, He F, et al. Identification of key genes and pathways in osteoarthritis via bioinformatic tools: an updated analysis[J]. Cartilage, 2021, 13(1_suppl): 1457S-1464S.
