ArticleFood science & nutrition2025
Ellagic Acid Modulates Necroptosis, Autophagy, Inflammations, and Stress to Ameliorate Nonalcoholic Liver Fatty Disease in a Rat Model.
Article in Food science & nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed.
- Ellagic Acid Attenuates CClCurrent issues in molecular biology · 2026Article
- Modulation of mRNA Expression of Biomarkers in the UPR-PERK Pathway by Ellagic Acid in Metabolic Dysfunction-Associated Fatty Liver Disease.International journal of molecular sciences · 2026Article
- Metabolic syndrome necroptosis: disease implications and therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Targeting necroptosis: how does exercise protect against metabolic dysfunction-associated fatty liver disease?Frontiers in physiology · 2026Review
- Targeting Lipophagy in Liver Diseases: Impact on Oxidative Stress and Steatohepatitis.Antioxidants (Basel, Switzerland) · 2025Review
- Cultural and Molecular Factors Predisposed to Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus.Nutrients · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) is considered one of the most common metabolic disorders worldwide. Although the pathoetiology of NAFLD is not fully elucidated, recent evidence suggests the involvement of stress, inflammation, and programmed death in the onset and progression of the disease. This investigation aimed to evaluate the effects of ellagic acid (EA), a known herbal antioxidant, on a high-fat diet (HFD)-induced animal model of NAFLD by evaluating the status of lipid profile, necroptosis (RIPK1, RIPK3, and MLKL), autophagy (LC3, ATG5, and BECN1), inflammation (TNF-α, IL-6, IL-4, and IL-10), and stress (SOD, CAT, GR, GPx, and MDA). In this regard, rats were randomly divided into 6 groups as follows: normal diet controls, HFD (supplemented with high caloric diet model), EA low dose (HFD and 10 mg/kg/day EA), EA middle dose (HFD and 25 mg/kg/day EA), EA high dose (HFD and 50 mg/kg/day EA), and Rosiglitazone (HFD and 10 mg/kg/day Rosi). After the treatment, the levels of markers related to necroptosis and autophagy in the liver tissue as well as the lipid profiles, inflammation, and oxidative stress status were analyzed. It was shown that the dose of EA was able to improve the weight gain and lipid profile when compared to NAFLD animals (
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