Icariin ameliorates LPS-induced acute lung injury in mice via complement C5a-C5aR1 and TLR4 signaling pathways.

Guo, J ; Zhang, QY ; et al.

In: International immunopharmacology, Jg. 131 (2024-04-20), S. 111802

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Acute lung injury (ALI) is an acute respiratory-related progressive disorder, which lacks specific pharmacotherapy. Icariin (ICA) has been shown to be effective in treating ALI. However, the targets and pharmacological mechanisms underlying the effects of ICA in the treatment of ALI are relatively lacking. Based on network pharmacology and molecular docking analyses, the gene functions and potential target pathways of ICA in the treatment of ALI were determined. In addition, the underlying mechanisms of ICA were verified by immunohistochemistry, immunofluorescence, quantitative Real-time PCR, and Western blot in LPS-induced ALI mice. The biological processes targeted by ICA in the treatment of ALI included the pathological changes, inflammatory response, and cell signal transduction. Network pharmacology, molecular docking, and in vivo experimental results revealed that ICA inhibited the complement C5a-C5aR1 axis, TLR4 mediated NF-κB, MAPK, and JAK2-STAT3 signaling pathways related gene and protein expressions, and decreased inflammatory cytokine, chemokine, adhesion molecule expressions, and mitochondrial apoptosis in LPS-induced ALI.

Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Titel:	Icariin ameliorates LPS-induced acute lung injury in mice via complement C5a-C5aR1 and TLR4 signaling pathways.
Autor/in / Beteiligte Person:	Guo, J ; Zhang, QY ; Xu, L ; Li, M ; Sun, QY
Link:	Zum Volltext
Zeitschrift:	International immunopharmacology, Jg. 131 (2024-04-20), S. 111802
Veröffentlichung:	Amsterdam ; New York : Elsevier Science, c2001-, 2024
Medientyp:	academicJournal
ISSN:	1878-1705 (electronic)
DOI:	10.1016/j.intimp.2024.111802
Schlagwort:	Animals Mice Lung pathology Molecular Docking Simulation NF-kappa B metabolism Signal Transduction Toll-Like Receptor 4 metabolism Acute Lung Injury drug therapy Acute Lung Injury metabolism Complement C5a metabolism Flavonoids therapeutic use Lipopolysaccharides pharmacology Receptors, Complement metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [Int Immunopharmacol] 2024 Apr 20; Vol. 131, pp. 111802. <i>Date of Electronic Publication: </i>2024 Mar 10. MeSH Terms: Acute Lung Injury* / drug therapy ; Acute Lung Injury* / metabolism ; Complement C5a* / metabolism ; Flavonoids* / therapeutic use ; Lipopolysaccharides* / pharmacology ; Receptors, Complement* / metabolism ; Animals ; Mice ; Lung / pathology ; Molecular Docking Simulation ; NF-kappa B / metabolism ; Signal Transduction ; Toll-Like Receptor 4 / metabolism Contributed Indexing: Keywords: Acute lung injury; Complement; Icariin; Inflammation; Mitochondrial apoptosis Substance Nomenclature: 80295-54-1 (Complement C5a) ; 0 (Flavonoids) ; VNM47R2QSQ (icariin) ; 0 (Lipopolysaccharides) ; 0 (NF-kappa B) ; 0 (Toll-Like Receptor 4) ; 0 (Receptors, Complement) Entry Date(s): Date Created: 20240311 Date Completed: 20240410 Latest Revision: 20240412 Update Code: 20240413

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