ArticleBMC complementary medicine and therapies2025
Luteolin ameliorates rat model of metabolic syndrome-induced cardiac injury by apoptosis suppression and autophagy promotion via NR4A2/p53 regulation.
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Luteolin Alleviates Axitinib-Induced Cardiomyocyte Apoptosis in Mice.Journal of biochemical and molecular toxicology · 2026Article
- Research Progress and Prospects of Flavonoids in the Treatment of Diseases by Regulating Autophagy: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
- Shenqi Granules Enhance Recovery from Myocardial Ischemia-Reperfusion Injury by Downregulating MMP9 and ADH1C.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Luteolin Relieves Metabolic Dysfunction-Associated Fatty Liver Disease Caused by a High-Fat Diet in Rats Through Modulating the AdipoR1/AMPK/PPARγ Signaling Pathway.International journal of molecular sciences · 2025Article
- Targeting the AMP-activated protein kinase pathway: the active metabolites of botanical drugs represent potential strategies for treating metabolic-associated fatty liver disease.Frontiers in pharmacology · 2025Review
- Research Progress on the Role and Mechanism of Flavonoids in Improving Metabolic Associated Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
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3 authors.
Funding
Abstract
backgroundReduced cardiac autophagy, inflammation, and apoptosis contribute to cardiovascular complications caused by metabolic syndrome (MetS). It is documented that the nuclear receptor 4A2 (NR4A2) could modulate autophagy and apoptosis in cardiac complications. The aim of this investigation was to assess the therapeutic potential of luteolin, with documented beneficial properties, against MetS-associated cardiac injury.
methodsForty male albino Wistar rats were divided into 5 groups randomly as controls, MetS, and MetS animals treated with luteolin (25, 50, 100 mg/kg ip). The animal's weight, blood pressure, lipid profile, tolerance to glucose and insulin, and cardiac histopathology were evaluated. Moreover, troponin T, creatine kinase-myocardial band (CK-MB), inflammatory profile (IL-6, IL-1β, TNF-α), transforming growth factor-β1 (TGF-β1), oxidative stress, and matrix metalloproteinase-9 (MMP-9) were analyzed to determine the cardiac state. Cardiac NR4A2 and p53, as well as apoptotic (B-cell leukemia/lymphoma 2 [BCL-2], Caspase [CASP]-3, and CASP-9) and autophagic mediators (Sequestosome-1/p62, Microtubule-associated protein 1 A/1B-light chain 3 [LC3], and Beclin-1) were measured by RT-qPCR and ELISA.
resultsLuteolin remarkably restored MetS-induced biochemical derangements and related cardiac injury via the suppression of apoptosis, inflammation, and stress but promotion of autophagy (p-value < 0.001).
conclusionCurrent findings revealed the promising therapeutical properties of luteolin against MetS-associated cardiovascular risks.
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