ArticleScientific reports2017
Honokiol suppresses formyl peptide-induced human neutrophil activation by blocking formyl peptide receptor 1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Anti-Inflammatory Saponins From an Edible Aquatic Plant Nymphoides hydrophylla.Phytochemical analysis : PCA · 2025Article
- Bioactive Compounds as Modulators of N-Formyl Peptide Signaling in Chronic Diseases.Molecules (Basel, Switzerland) · 2025Review
- Druggable targets for the immunopathy of Alzheimer's disease.RSC medicinal chemistry · 2023Review
- A fluorescent photoaffinity probe for formyl peptide receptor 1 labelling in living cells.RSC chemical biology · 2023Article
- Article
- Targeting Neutrophils to Treat Acute Respiratory Distress Syndrome in Coronavirus Disease.Frontiers in pharmacology · 2020Review
- A novel NOX2 inhibitor attenuates human neutrophil oxidative stress and ameliorates inflammatory arthritis in mice.Redox biology · 2019Article
- The formyl peptide fMLF primes platelet activation and augments thrombus formation.Journal of thrombosis and haemostasis : JTH · 2019Article
- SIRT3 activator honokiol ameliorates surgery/anesthesia-induced cognitive decline in mice through anti-oxidative stress and anti-inflammatory in hippocampus.CNS neuroscience & therapeutics · 2019Article
- FPR1 mediates the tumorigenicity of human cervical cancer cells.Cancer management and research · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formyl peptide receptor 1 (FPR1) mediates bacterial and mitochondrial N-formyl peptides-induced neutrophil activation. Therefore, FPR1 is an important therapeutic target for drugs to treat septic or sterile inflammatory diseases. Honokiol, a major bioactive compound of Magnoliaceae plants, possesses several anti-inflammatory activities. Here, we show that honokiol exhibits an inhibitory effect on FPR1 binding in human neutrophils. Honokiol inhibited superoxide anion generation, reactive oxygen species formation, and elastase release in bacterial or mitochondrial N-formyl peptides (FPR1 agonists)-activated human neutrophils. Adhesion of FPR1-induced human neutrophils to cerebral endothelial cells was also reduced by honokiol. The receptor-binding results revealed that honokiol repressed FPR1-specific ligand N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys-fluorescein binding to FPR1 in human neutrophils, neutrophil-like THP-1 cells, and hFPR1-transfected HEK293 cells. However, honokiol did not inhibit FPR2-specific ligand binding to FPR2 in human neutrophils. Furthermore, honokiol inhibited FPR1 agonist-induced calcium mobilization as well as phosphorylation of p38 MAPK, ERK, and JNK in human neutrophils. In conclusion, our data demonstrate that honokiol may have therapeutic potential for treating FPR1-mediated inflammatory diseases.
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