Trial reportFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Flavones induce neutrophil apoptosis by down-regulation of Mcl-1 via a proteasomal-dependent pathway.
Trial report in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Insights into the Pharmacological Effects of Flavonoids: The Systematic Review of Computer Modeling.International journal of molecular sciences · 2022Pooled it
- Real-time characterisation of microbe-induced inflammation using a novel zebrafish larval corneal injury and infection model.Communications biology · 2026Article
- Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025Review
- The role of neutrophil-to-lymphocyte ratio in the prognosis of chronic kidney disease: insights from the NHANES cohort study.Frontiers in systems biology · 2025Article
- Luteolin as a multifaceted immunomodulator: insights into its effects on diverse immune cell populations and therapeutic implications.Frontiers in immunology · 2025Review
- Article
- Inflammation and Obesity: The Pharmacological Role of Flavonoids in the Zebrafish Model.International journal of molecular sciences · 2023Review
- Application of transgenic zebrafish for investigating inflammatory responses to nanomaterials: Recommendations for new users.F1000Research · 2023Review
- A retrospective study of Pupingqinghua prescription versus Lianhuaqingwen in Chinese participants infected with SARS-CoV-2 Omicron variants.Frontiers in pharmacology · 2022Article
- Zebrafish as a Useful Model to Study Oxidative Stress-Linked Disorders: Focus on Flavonoids.Antioxidants (Basel, Switzerland) · 2021Review
- Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation.Thorax · 2020Article
- Therapeutic Potential of Flavonoids in Pain and Inflammation: Mechanisms of Action, Pre-Clinical and Clinical Data, and Pharmaceutical Development.Molecules (Basel, Switzerland) · 2020Review
- Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocyte-dendritic cell antigen presentation.Science immunology · 2019Article
- ROCK Inhibition Drives Resolution of Acute Inflammation by Enhancing Neutrophil Apoptosis.Cells · 2019Article
- Inflammation Resolution and the Induction of Granulocyte Apoptosis by Cyclin-Dependent Kinase Inhibitor Drugs.Frontiers in pharmacology · 2019Review
- Mer-mediated eosinophil efferocytosis regulates resolution of allergic airway inflammation.The Journal of allergy and clinical immunology · 2018Article
- The significant impact of apigenin on different aspects of autoimmune disease.Inflammopharmacology · 2018Review
- Blood Neutrophils Are Reprogrammed in Bronchiectasis.American journal of respiratory and critical care medicine · 2018Article
- Palmitic acid, but not high-glucose, induced myocardial apoptosis is alleviated by N‑acetylcysteine due to attenuated mitochondrial-derived ROS accumulation-induced endoplasmic reticulum stress.Cell death & disease · 2018Article
- Wogonin attenuates nasal polyp formation by inducing eosinophil apoptosis through HIF-1α and survivin suppression.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Neutrophil apoptosis and subsequent nonphlogistic clearance by surrounding phagocytes are key to the successful resolution of neutrophilic inflammation, with dysregulated apoptosis reported in multiple human inflammatory diseases. Enhancing neutrophil apoptosis has proresolution and anti-inflammatory effects in preclinical models of inflammation. Here we investigate the ability of the flavones apigenin, luteolin, and wogonin to induce neutrophil apoptosis in vitro and resolve neutrophilic inflammation in vivo. Human neutrophil apoptosis was assessed morphologically and by flow cytometry following incubation with apigenin, luteolin, and wogonin. All three flavones induced time- and concentration-dependent neutrophil apoptosis (apigenin, EC=12.2 μM; luteolin, EC=14.6 μM; and wogonin, EC=28.9 μM). Induction of apoptosis was caspase dependent, as it was blocked by the broad-spectrum caspase inhibitor Q-VD-OPh and was associated with both caspase-3 and caspase-9 activation. Flavone-induced apoptosis was preceded by down-regulation of the prosurvival protein Mcl-1, with proteasomal inhibition preventing flavone-induced Mcl-1 down-regulation and apoptosis. The flavones abrogated the survival effects of mediators that prolong neutrophil life span, including lipoteichoic acid, peptidoglycan, dexamethasone, and granulocyte-macrophage colony stimulating factor, by driving apoptosis. Furthermore, wogonin enhanced resolution of established neutrophilic inflammation in a zebrafish model of sterile tissue injury. Wogonin-induced resolution was dependent on apoptosis in vivo as it was blocked by caspase inhibition. Our data show that the flavones induce neutrophil apoptosis and have potential as neutrophil apoptosis-inducing anti-inflammatory, proresolution agents.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.