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基于网络药理学和动物实验探讨血必净注射液治疗急性呼吸窘迫综合征的作用机制
Authors Li J, Shen M, Yin Z
Received 17 December 2024
Accepted for publication 26 April 2025
Published 7 May 2025 Volume 2025:18 Pages 6037—6047
DOI http://doi.org/10.2147/JIR.S507468
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tara Strutt
Jin Li,1,* Meirong Shen,2,* Zuan Yin3
1Department of Intensive Care Unit, The Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang City, Jiangxi Province, 330006, People’s Republic of China; 2Department of Intensive Care Unit, Ganzhou People’s Hospital, Ganzhou City, Jiangxi Province, 341000, People’s Republic of China; 3Department of Emergency, Jiangxi Provincial People’s Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang City, Jiangxi Province, 330006, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Zuan Yin, Department of Emergency, Jiangxi Provincial People’s Hospital, 152 Aiguo Road, Donghu District, Nanchang City, Jiangxi Province, 330006, People’s Republic of China, Email yuzan201709@126.com
Objective: To explore the mechanism of Xuebijing injection (XBJ) in treating acute respiratory distress syndrome (ARDS) using network pharmacology and animal experiments.
Methods: Active ingredients of XBJ were analyzed via TCMSP, and ARDS-related targets were identified through DisGENET and Genecard. Intersection targets were obtained using PubChem and Venn diagrams. Protein interaction networks, GO, and KEGG enrichment analyses were conducted. An ARDS rat model was established using lipopolysaccharide (LPS), and rats were divided into control, LPS, and XBJ-treated groups (low, medium, high doses, n=10). Lung wet/dry (W/D) ratio, inflammatory cytokines (IL-17, IL-6, IL-1β, TNF-α), MPO levels, lung pathology, and protein expression of ICAM-1 and HIF-1α were assessed via ELISA, HE staining, immunohistochemistry, and Western blot.
Results: A total of 204 ARDS targets were identified, with 46 intersection targets, mainly TNF-α, MPO, HIF-1α, and ICAM-1. XBJ affected ARDS through IL-17, HIF-1, and TNF signaling pathways. In vivo, LPS-induced lung injury showed alveolar destruction, edema, and inflammation, with increased W/D ratio, cytokines, MPO, and protein expression of HIF-1α and ICAM-1 (P< 0.05). XBJ treatment alleviated lung damage, reduced inflammation, and improved pathology in a dose-dependent manner (P< 0.05).
Conclusion: XBJ alleviates ARDS by regulating immune function, oxidative stress, and inflammation through IL-17, HIF-1, and TNF pathways.
Keywords: network pharmacology, Xuebijing injection, acute respiratory distress syndrome, lipopolysaccharide