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Selenium Nanoparticles Inhibited H2O2-Induced Endothelial Cell Dysfunction by Alleviating Oxidative Stress.
Na Li1, Shengze Xiao1, Wanru Yang1
1Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan, China.
Biological Trace Element Research
|June 27, 2026
Summary
Selenium nanoparticles (SeNPs) protect against endothelial dysfunction by reducing oxidative stress. Middle-sized SeNPs (around 40 nm) were most effective, enhancing cellular selenium uptake and antioxidant expression, suggesting potential therapeutic use for atherosclerosis.
Area of Science:
- Biomedical Engineering
- Nanomedicine
- Cardiovascular Research
Background:
- Endothelial dysfunction is a key factor in atherosclerosis, a leading cause of death.
- Selenium nanoparticles (SeNPs) previously showed potential in preventing atherosclerosis, but their effect on endothelial dysfunction was unclear.
- Nanomaterial size and surface properties significantly impact biological activity.
Purpose of the Study:
- To investigate the effects of different sized SeNPs on hydrogen peroxide (H2O2)-induced endothelial dysfunction.
- To elucidate the underlying mechanisms of SeNPs' protective action against endothelial dysfunction.
- To determine the optimal size of SeNPs for mitigating endothelial dysfunction.
Main Methods:
- Preparation of SeNPs with varying sizes (approx. 20, 40, and 80 nm) and surface charges.
- Induction of endothelial dysfunction using H2O2 in endothelial cells.
- Assessment of cell viability, oxidative stress markers, cellular selenium content, and selenoprotein expression.
- Analysis of the Nrf2/Keap1 signaling pathway.
Main Results:
- SeNPs pretreatment significantly reduced H2O2-induced endothelial cell injury and dysfunction.
- SeNPs inhibited oxidative stress by increasing cellular selenium and antioxidant selenoprotein expression.
- SeNPs modulated the Nrf2/Keap1 pathway, and middle-sized SeNPs (approx. 40 nm) showed superior efficacy in cellular uptake and antioxidant induction.
- The protective effect of SeNPs against endothelial dysfunction was dependent on particle size.
Conclusions:
- SeNPs protect endothelial cells from H2O2-induced dysfunction by alleviating oxidative stress.
- The anti-endothelial dysfunction activity of SeNPs is influenced by their particle size, with middle-sized nanoparticles being most effective.
- These findings support the potential of SeNPs as a therapeutic strategy for atherosclerosis.
