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This study aims to evaluate the effectiveness of EGCG-functionalized selenium nanoparticles in reducing hepatic damage caused by a high-fat diet.

June 28, 2026International Journal of Molecular Sciences2 citationsOpen Access

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EGCG-Functionalized Selenium Nanoparticles Mitigate High-Fat Diet-Induced Hepatic Lipotoxicity Through Keap1/Nrf2 Redox Modulation and Transcriptional Regulation of AMPK/SIRT1/PGC-1α/MFN2-Associated Mitochondrial Homeostasis

FSFatma Al-Zahraa Sayed MMMennat allah Maher MEMariam Elsayed Elborlosy

Key Points

This study aims to evaluate the effectiveness of EGCG-functionalized selenium nanoparticles in reducing hepatic damage caused by a high-fat diet.
Forty-two adult male rats were divided into six groups: control, high-fat diet (HFD), HFD with Lipanthyl, HFD with EGCG, HFD with sodium selenite, and HFD with EGCG-SeNPs.
Various analyses including dynamic light scattering, transmission electron microscopy, and assessments of lipid profile and biomarkers were performed post-intervention.
HFD was induced in the rats to observe changes in metabolic conditions and associated oxidative and inflammatory responses.
EGCG-SeNPs improved lipid profiles significantly compared to HFD alone, with a notable reduction in hepatic enzymes and cardiac injury biomarkers.
Antioxidant status was enhanced, while inflammatory markers and apoptotic markers showed significant reduction; for example, TNF-α levels decreased (exact data not specified).
Histological analyses indicated improved hepatic architecture and increased Nrf2 immunoreactivity.

Abstract

High-fat diet (HFD)-induced hyperlipidemia is an experimental metabolic condition characterized primarily by dysregulated serum lipid levels and hepatic lipid accumulation, with associated oxidative, inflammatory, mitochondrial, and cardiovascular alterations. This study investigated the therapeutic efficacy of epigallocatechin gallate (EGCG)-functionalized selenium nanoparticles (EGCG-SeNPs) against HFD-induced metabolic and hepatic injury, in comparison with free EGCG, sodium selenite (Na2SeO3), and Lipanthyl. EGCG-SeNPs were characterized by dynamic light scattering, zeta potential analysis, transmission electron microscopy, X-ray diffraction, and UV–visible spectrophotometry. Forty-two adult male rats were allocated into six groups: control, HFD, HFD/Lipanthyl, HFD/EGCG, HFD/Na2SeO3, and HFD/EGCG-SeNPs. High-fat diet (HFD) feeding induced pronounced dyslipidemia, elevated hepatic enzymes, increased cardiac injury biomarkers, enhanced lipid peroxidation and nitrosative stress, depletion of antioxidant defenses, and disruption of the Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2 (Keap1/Nrf2) regulatory axis. HFD also increased nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), while altering mitochondrial apoptotic markers, including B-cell lymphoma 2 (Bcl-2), cytochrome c, and caspase-3. At the transcriptional level, HFD increased lipogenic gene expression and reduced the expression of genes related to fatty-acid oxidation, metabolic regulation, and mitochondrial homeostasis. EGCG-SeNPs showed the greatest overall improvement among the tested interventions, as indicated by an improved lipid profile, hepato-cardiac injury biomarkers, antioxidant status, inflammatory markers, apoptotic markers, hepatic architecture, and Nrf2 immunoreactivity. Collectively, EGCG-SeNPs may mitigate HFD-induced hepatic lipotoxicity and associated cardiac stress through coordinated modulation of lipid metabolism, redox balance, inflammation, and mitochondrial homeostasis.

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EGCG-Functionalized Selenium Nanoparticles Mitigate High-Fat Diet-Induced Hepatic Lipotoxicity Through Keap1/Nrf2 Redox Modulation and Transcriptional Regulation of AMPK/SIRT1/PGC-1α/MFN2-Associated Mitochondrial Homeostasis

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