Frontiers in Bioengineering and Biotechnology (Jun 2021)

RETRACTED: Amorphous Selenium Nanoparticles Improve Vascular Function in Rats With Chronic Isocarbophos Poisoning via Inhibiting the Apoptosis of Vascular Endothelial Cells

  • Moli Zhu,
  • Moli Zhu,
  • Moli Zhu,
  • Zhitao Gao,
  • Yutian Fu,
  • Yue Qiu,
  • Keke Huang,
  • Chaonan Zhu,
  • Yinan Wu,
  • Tiantian Zhu,
  • Qianqian Wang,
  • Lin Yang,
  • Lin Yang,
  • Yaling Yin,
  • Peng Li

DOI
https://doi.org/10.3389/fbioe.2021.673327
Journal volume & issue
Vol. 9

Abstract

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AimThis study aimed to investigate the preventive effect and possible mechanism of amorphous selenium nanoparticles (A-SeQDs) on isocarbophos induced vascular dysfunction.MethodsA-SeQDs was made by auto redox decomposition of selenosulfate precursor. Male rats were given isocarbophos (0.5 mg/kg/2 days) by intragastric administration for 16 weeks to induce vascular dysfunction. During the course, A-SeQDs (50 mg/kg/day) was added to the water from week 5. Then, the rats were killed to observe and test the influence of A-SeQDs on the vascular dysfunction induced by isocarbophos. Finally, human umbilical vein endothelial cells (HUVECs) were treated with 10% DMEM of isocarbophos (100 μM) for 5 days to detect the related indexes. Before the use of isocarbophos treatment, different drugs were given.ResultsA-SeQDs could reduce total carbon dioxide, MDA, VCAM-1, ICAM-1, IL-1, and IL-6 while increasing oxygen saturation, NO content, and SOD activity in rats. A-SeQDs also resulted in relatively normal vascular morphology, and the expression of sodium hydrogen exchanger 1 (NHE1) and caspase-3 decreased in rats. Furthermore, in HUVECs treated with isocarbophos, A-SeQDs maintained mitochondrial membrane potential, inhibited the cleaved caspase-3 expression, and released cytochrome c from mitochondria to cytosol.ConclusionA-SeQDs can inhibit the apoptosis of HUVECs through the mitochondrial pathway, and effectively treat the impairment of vascular endothelial function caused by isocarbophos, which is NHE1-dependent.

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