ArticleYonsei medical journal2022
Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3.
Article in Yonsei medical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Research Progress and Prospects of Flavonoids in the Treatment of Diseases by Regulating Autophagy: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
- Adipose-derived regenerative cell therapy mitigates sepsis-induced cardiomyopathy through the induction of cardiac reparative lymphangiogenesis.Stem cell research & therapy · 2026Article
- NETosis in Alzheimer's Disease: Understanding the Role of Neutrophil Extracellular Traps (NETs) in Neuroinflammation and Disease Pathogenesis.Molecular neurobiology · 2025Review
- Protective effects of luteolin on high glucose-induced ferroptosis in müller cells.International ophthalmology · 2025Article
- Luteolin: exploring its therapeutic potential and molecular mechanisms in pulmonary diseases.Frontiers in pharmacology · 2025Review
- The regulatory effects of luteolin, calycosin, and formononetin on the NLRP3/IL-33/ILC2s axis in the treatment of allergic rhinitis: mechanistic analysis and therapeutic potential.Frontiers in pharmacology · 2025Review
- Yohimbine Treatment Alleviates Cardiac Inflammation/Injury and Improves Cardiac Hemodynamics by Modulating Pro-Inflammatory and Oxidative Stress Indicators.Inflammation · 2024Article
- Effect of luteolin on oxidative stress and inflammation in the human osteoblast cell line hFOB1.19 in an inflammatory microenvironment.BMC pharmacology & toxicology · 2024Article
- Flavonoids, gut microbiota, and host lipid metabolism.Engineering in life sciences · 2024Review
- NLRP3 exacerbates EAE severity through ROS-dependent NET formation in the mouse brain.Cell communication and signaling : CCS · 2024Article
- A Comprehensive Review of the Phytochemical Constituents and Bioactivities ofTheScientificWorldJournal · 2024Review
- NLRP3 Exacerbate NETosis-Associated Neuroinflammation in an LPS-Induced Inflamed Brain.Immune network · 2023Article
- Immunopharmacological Activities of Luteolin in Chronic Diseases.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn this article, we aimed to investigate the influences of luteolin on inflammatory injury to cardiomyocytes induced by lipopolysaccharide (LPS). MATERIALS AND
methodsH9c2 cells were pretreated with different concentrations of luteolin (10, 20, and 50 µM) for 12 h and then stimulated with 10 µg/mL LPS or no LPS for 6 h. Cell viability was detected by CCK-8 assay. Cell apoptosis was determined by flow cytometry. QRT-PCR and Western blotting were utilized to examine mRNA and protein levels. ELISA was used to determine the levels of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin (IL)-6, IL-1β, and IL-18 in cell supernatants among different groups of H9c2 cells. Immunofluorescence was applied to evaluate reactive oxygen species formation in H9c2 cells. M-mode images of echocardiography, the ejection fraction test, fractional shortening test, end-systolic volume test, and end-diastolic volume test of mouse heart function were obtained by ultrasonic electrocardiogram.
resultsLuteolin could alleviate inflammatory damage and inflammatory factor expression among LPS-induced H9c2 cells. Additionally, we found that luteolin decreased LPS-stimulated inflammatory damage in H9c2 cells by down-regulating NOD-like receptor family pyrin domain containing 3 (Nlrp3). Luteolin also improved myocardial function in mice treated with LPS and reduced myocardial relaxation. Luteolin reversed myocardial histological abnormalities in mice and reduced inflammation and cardiomyocyte apoptosis. Additionally, luteolin inhibited oxidative stress-mediated myocardial and systemic tissue damage in mice. Finally, luteolin reduced LPS-induced inflammatory damage in mouse cardiomyocytes by down-regulating Nlrp3.
conclusionWe found that luteolin could reduce inflammatory damage to cardiomyocytes induced by LPS by down-regulating Nlrp3.
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