Tissue & cell · 2026
Quercetin-mediated selenium nanoparticles protect against hyperthyroidism-induced hepatic injury: Involvement of Nrf2/NF-κB signaling, mitochondrial apoptosis, and iron/heme imbalance.
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Ali Mohamed A, Alam-ELDein Khaled M, Elsayed Ganna Adel, Ghareeb Mariam, Hesham Roaa, Ali Haya Ashraf, Abdelaal Rawan Magdy, Mahyoub Baraa Abdo, Elshafey Moaz M, Fayad Eman, Alsyaad Khalid M, Alsunbul Maha, Gadelmawla Mohamed H A
Аннотация
PURPOSE: Hyperthyroidism-associated liver injury represents an important extra-thyroidal complication of thyroid hormone excess, driven by increased metabolic demand and interconnected oxidative, inflammatory, and mitochondrial disturbances. However, the coordinated involvement of Nrf2/NF-κB signaling, apoptosis, and iron/heme dysregulation remains insufficiently understood, highlighting the need for hepatoprotective strategies. Therefore, this study evaluated the hepatoprotective efficacy of quercetin-mediated selenium nanoparticles (QUR-SeNPs) against L-thyroxine-induced hyperthyroidism in rats and compared their effects with free quercetin and sodium selenite.
METHODS: QUR-SeNPs were synthesized and characterized using dynamic light scattering, zeta potential analysis, and transmission electron microscopy. Forty male albino rats were divided into five groups: Normal, hyperthyroid (HPT), HPT&Na₂SeO₃, HPT&QUR, and HPT&QUR-SeNPs. Thyroid hormone profile, liver function biomarkers, oxidative/antioxidant status, inflammatory mediators, apoptotic markers, iron homeostasis, hepatic iron/heme-related gene expression, Nrf2 immunoexpression, and histopathological alterations were assessed.
RESULTS: L-thyroxine induced a hyperthyroid state associated with hepatic dysfunction, oxidative/nitrosative stress, impaired Nrf2/Nfe2l2 antioxidant signaling, NF-κB-mediated inflammation, mitochondrial apoptotic activation, and disrupted systemic and hepatic iron homeostasis. QUR-SeNPs markedly improved the circulating thyroid hormone profile, improved liver enzyme activities, reduced NO, MDA, and Keap-1, enhanced GSH and antioxidant enzymes, suppressed TNF-α, IL-6, COX-2, and NF-κB, and normalized Bax/Bcl-2/caspase-3 signaling. Moreover, QUR-SeNPs corrected iron imbalance, regulated Hamp1, Tfr1, Ftl, ALAS1, and HRI expression, restored Nrf2 immunoexpression, and improved hepatic histoarchitecture.
CONCLUSION: QUR-SeNPs exerted greater modulating the Nrf2/NF-κB pathways role in hepatoprotection compared with free quercetin and sodium selenite, suggesting their therapeutic promise against hyperthyroidism-induced liver injury through coordinated regulation of redox, inflammatory, apoptotic, and iron/heme metabolic pathways.
METHODS: QUR-SeNPs were synthesized and characterized using dynamic light scattering, zeta potential analysis, and transmission electron microscopy. Forty male albino rats were divided into five groups: Normal, hyperthyroid (HPT), HPT&Na₂SeO₃, HPT&QUR, and HPT&QUR-SeNPs. Thyroid hormone profile, liver function biomarkers, oxidative/antioxidant status, inflammatory mediators, apoptotic markers, iron homeostasis, hepatic iron/heme-related gene expression, Nrf2 immunoexpression, and histopathological alterations were assessed.
RESULTS: L-thyroxine induced a hyperthyroid state associated with hepatic dysfunction, oxidative/nitrosative stress, impaired Nrf2/Nfe2l2 antioxidant signaling, NF-κB-mediated inflammation, mitochondrial apoptotic activation, and disrupted systemic and hepatic iron homeostasis. QUR-SeNPs markedly improved the circulating thyroid hormone profile, improved liver enzyme activities, reduced NO, MDA, and Keap-1, enhanced GSH and antioxidant enzymes, suppressed TNF-α, IL-6, COX-2, and NF-κB, and normalized Bax/Bcl-2/caspase-3 signaling. Moreover, QUR-SeNPs corrected iron imbalance, regulated Hamp1, Tfr1, Ftl, ALAS1, and HRI expression, restored Nrf2 immunoexpression, and improved hepatic histoarchitecture.
CONCLUSION: QUR-SeNPs exerted greater modulating the Nrf2/NF-κB pathways role in hepatoprotection compared with free quercetin and sodium selenite, suggesting their therapeutic promise against hyperthyroidism-induced liver injury through coordinated regulation of redox, inflammatory, apoptotic, and iron/heme metabolic pathways.