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Nephroprotective Effects of Selenium Nanoparticles Against Sodium Arsenite-Induced Damages

INTRODUCTION: The potential effects of selenium nanoparticles (SeNPs) administration on arsenic exposure-mediated nephrotoxicity by alleviating fibrosis, inflammation, oxidative stress-related damage, and apoptosis remains more detailed investigations. METHODS: After the synthesis of selenium nanopa...

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Detalles Bibliográficos
Autores principales: Li, Shubin, Dong, Xingna, Xu, Limeng, Wu, Zhenli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10276609/
https://www.ncbi.nlm.nih.gov/pubmed/37333733
http://dx.doi.org/10.2147/IJN.S413362
Descripción
Sumario:INTRODUCTION: The potential effects of selenium nanoparticles (SeNPs) administration on arsenic exposure-mediated nephrotoxicity by alleviating fibrosis, inflammation, oxidative stress-related damage, and apoptosis remains more detailed investigations. METHODS: After the synthesis of selenium nanoparticles (SeNPs) by sodium selenite (Na(2)SeO(3)) through a versatile and green procedure, the biosafety of SeNPs was assessed by assaying renal functions and inflammation in mice. Subsequently, nephroprotective effects of SeNPs against sodium arsenite (NaAsO(2))-induced damages were confirmed by biochemical, molecular, and histopathological assays, including renal function, histological lesion, fibrosis, inflammation, oxidative stress-related damage, and apoptosis in mice renal tissues and renal tubular duct epithelial cells (HK2 cells). RESULTS: The excellent biocompatibility and safety of SeNPs prepared in this study were confirmed by the non-significant differences in the renal functions and inflammation levels in mice between the negative control (NC) and 1 mg/kg SeNPs groups (p>0.05). The results of biochemical, molecular, and histopathological assays confirmed that daily administration of 1 mg/kg SeNPs for 4 weeks not only ameliorated renal dysfunctions and injuries caused by NaAsO(2) exposure but also inhibited the fibrosis, inflammation, oxidative stress-related damage, and apoptosis in the renal tissues of NaAsO(2)-exposed mice. In addition, altered viability, inflammation, oxidative stress-related damage, and apoptosis in the NaAsO(2)-exposed HK2 cells were effectively reversed after 100 μg/mL SeNPs supplementation. CONCLUSION: Our findings authentically confirmed the biosafety and nephroprotective effects of SeNPs against NaAsO(2) exposure-induced damages by alleviating inflammation, oxidative stress-related damage, and apoptosis.