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Ameliorative Effect of Sodium Selenite on Silver Nanoparticles-Induced Myocardiocyte Structural Alterations in Rats

Authors
  • Ma, Wanrui1, 2
  • He, Shan3
  • Xu, Yanping1
  • Qi, Guoxue3
  • Ma, Huiyan3
  • Bang, John J4
  • Li, P Andy2
  • 1 General Hospital of Ningxia Medical University, Yinchuan, Ningxia
  • 2 Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, Durham, NC
  • 3 Ningxia Medical University, Yinchuan, Ningxia
  • 4 Earth and Geospatial Sciences, North Carolina Central University, Durham, NC
Type
Published Article
Journal
International Journal of Nanomedicine
Publisher
Dove Medical Press
Publication Date
Oct 27, 2020
Volume
15
Pages
8281–8292
Identifiers
DOI: 10.2147/IJN.S271457
PMID: 33149575
PMCID: PMC7603418
Source
PubMed Central
Keywords
License
Green

Abstract

Background The application of silver nanoparticles (AgNPs) is growing exponentially, and its potential damage to the cardiac remains to be elucidated. The purpose of this study was to investigate the ameliorative effect of sodium selenite on silver nanoparticles-induced myocardiocyte structural alterations in rats. Materials and Methods Forty male Sprague-Dawley (SD) rats were randomly divided into four groups: control group, AgNPs group, Se control group, and AgNPs + Se group. SD rats were administered AgNPs through a single intratracheal instillation, and sodium selenite was given by intraperitoneal injection for seven days. Cardiac function was determined by echocardiography and hemodynamic, ultrastructural changes by transmission electron microscopy examination. Mitochondrial fission and autophagy markers were measured by Western blotting. Results AgNPs caused a significant decrease in cardiac contraction, diastolic dysfunction, fragmentation, and lysis of the myofibrils, the formation of stenosis in the capillary, damaging the mitochondria membrane and cristae. AgNPs significantly increased mitochondrial fission markers dynamin-related protein 1 (Drp1), phospho-Drp1 (p-Drp1), and mitochondrial fission protein 1 (Fis1), as well as autophagy marker LC3 II/I ( P <0.05). Treatment with sodium selenite is capable of protecting cardiac function from AgNPs toxicity through attenuating ultrastructural alterations, stabilizing mitochondrial dynamic balance and blocking mitochondrial autophagy. Conclusion We conclude that the protection of sodium selenite against silver nanoparticles-induced myocardiocyte structural alterations is associated with stabilizing mitochondrial dynamic balance and mitophagy.

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