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Anti-Oxidant and Anti-Endothelial Dysfunctional Properties of Nano-Selenium in vitro and in vivo of Hyperhomocysteinemic Rats

Authors Zheng Z, Liu L, Zhou K, Ding L, Zeng J, Zhang W

Received 31 March 2020

Accepted for publication 25 May 2020

Published 23 June 2020 Volume 2020:15 Pages 4501—4521

DOI https://doi.org/10.2147/IJN.S255392

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Lei Yang


Zeqi Zheng,1,* Lijuan Liu,1,* Kaiwen Zhou,2,* Lu Ding,1,3 Junyi Zeng,1,3 Wan Zhang1,3

1Department of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, People’s Republic of China; 2The First Clinical Medical College, School of Medicine, Nanchang University, Nanchang, Jiangxi 330006, People’s Republic of China; 3Jiangxi Hypertension Research Institute, Nanchang, Jiangxi 330006, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Wan Zhang
Department of Cardiology, The First Affiliated Hospital of Nanchang University; Jiangxi Hypertension Research Institute, Nanchang, Jiangxi 330006, People’s Republic of China
Tel +86-15907086833
Fax +86-0791-88692748
Email wanzhang@ncu.edu.cn

Purpose: Elevation of blood homocysteine (Hcy) level (hyperhomocysteinemia) is a risk factor for cardiovascular disorders and is closely associated with endothelial dysfunction. The present study aims to investigate the protective effect and underlying mechanism of nanoscale selenium (Nano-Se) in Hcy-mediated vascular endothelial cell dysfunction in vitro and in vivo.
Materials and Methods: By incubating vascular endothelial cells with exogenous Hcy and generating hyperhomocysteinemic rat model, the effects of Nano-Se on hyperhomocysteinemia-mediated endothelial dysfunction and its essential mechanisms were investigated.
Results: Nano-Se inhibited Hcy-induced mitochondrial oxidative damage and apoptosis by preventing the downregulation of glutathione peroxidase enzyme 1 and 4 (GPX1, GPX4) in the vascular endothelial cells, thus effectively prevented the vascular damage in vitro and in vivo in the hyperhomocysteinemic rats. Nano-Se possessed similar protective effects but lower toxicity against Hcy in vascular endothelial cells when compared with other forms of Se.
Conclusion: The application of Nano-Se could serve as a novel promising strategy against Hcy-mediated vascular dysfunction with reduced risk of Se toxicity.

Keywords: nano-selenium, Nano-Se, homocysteine, endothelium dysfunction, glutathione peroxidase enzymes, GPXs, reactive oxygen species, ROS

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