ArticleMolecular medicine reports2019
Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Qishen Huoxue Granule Ameliorates LPS-induced Cardiomyocyte Injury by Suppressing Excessive AutophagyCombinatorial chemistry & high throughput screening · 2026Article
- Comprehensive review of biosynthesis, plant function, metabolism and new therapeutic bioactivities of flavonoids.ADMET & DMPK · 2026Review
- Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies.Food science & nutrition · 2025Review
- The Protective Effect of Flavonoids in the Diet on Autophagy-Related Cardiac Impairment.Nutrients · 2024Review
- Beneficial effects of flavonoids on cardiovascular diseases by influencing NLRP3 inflammasome.Inflammopharmacology · 2023Review
- A high-throughput drug screening identifies luteolin as a therapeutic candidate for pathological cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Article
- Article
- Potential mechanisms of Qili Qiangxin capsule to prevent pulmonary arterial hypertension based on network pharmacology analysis in a rat model.Annals of translational medicine · 2022Article
- Inhibition of PI3K/AKT/mTOR Signalling Pathway Activates Autophagy and Suppresses Peritoneal Fibrosis in the Process of Peritoneal Dialysis.Frontiers in physiology · 2022Article
- Fatty acid-binding protein 4 silencing protects against lipopolysaccharide-induced cardiomyocyte hypertrophy and apoptosis by inhibiting the Toll-like receptor 4-nuclear factor-κB pathway.The Journal of international medical research · 2021Article
- Mitoprotective Effects of a Synergistic Nutraceutical Combination: Basis for a Prevention Strategy Against Alzheimer's Disease.Frontiers in aging neuroscience · 2021Article
- [Role of autophagy in lipopolysaccharide-induced apoptosis of odontoblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Luteolin (LTL) serves essential roles in a wide variety of biological processes. Lipopolysaccharide (LPS) can lead to myocardial hypertrophy and autophagy. However, the roles of LTL on LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes have not yet been fully elucidated. In the present study, the morphology of cultured rat cardiomyocytes was observed under an inverted microscope. Cell viability was detected by MTT assay. α‑Actinin and microtubule‑associated protein 1 light chain 3 (LC3) expression levels were measured by immunofluorescence assay. In addition, the expression levels of atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP), LC3, and autophagy‑ and Wnt signaling pathway‑associated genes were analyzed by reverse transcription‑quantitative polymerase chain reaction or western blot assays. The results indicated that LTL increased the cell viability of cardiomyocytes treated with LPS. LTL decreased the expression of cardiac hypertrophy associated markers (ANP and BNP). LTL decreased α‑actinin and LC3 expression levels in LPS‑treated cardiomyocytes. It was also demonstrated that LTL suppressed the mRNA and protein expression levels of LPS‑mediated autophagy and Wnt signaling pathway‑associated genes. In addition, it was demonstrated that silencing of β‑catenin inhibited LPS‑induced cardiomyocyte hypertrophy and the formation of autophagosomes. Thus, the present study suggested that LTL protected against LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes.
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