International Journal of Medical Sciences

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21 November 2018

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Int J Med Sci 2018; 15(10):978-985. doi:10.7150/ijms.24659

Research Paper

Endothelial-cell inflammation and damage by reactive oxygen species are prevented by propofol via ABCA1-mediated cholesterol efflux

Chih-Peng Hsu1#, Chih-Hung Lin2#, Chan-Yen Kuo3,4✉

1. Department of Cardiology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan
2. Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan
3. Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chungli, Taiwan
4. Department of Ophthalmology, Hsin Sheng Junior College of Medical Care and Management, Longtan, Taiwan
# The first two authors contributed equally to this work

Abstract

Background: Cholesterol efflux efficiency, reactive oxygen species, and inflammation are closely related to cardiovascular diseases. Our aim was to investigate the effect of propofol on cholesterol-loaded rat aortic endothelial cells after high-density lipoprotein treatment in vitro.

Methods and Results: The results showed that propofol promoted cholesterol efflux and ameliorated inflammation and reactive oxygen species overproduction according to the analysis of p65 nuclear translocation and a 2′,7′-dichlorofluorescin diacetate assay, respectively.

Conclusions: These results provide a possible explanation for the anti-inflammatory, antioxidant, and cholesterol efflux-promoting effects of propofol on rat aortic endothelial cells after incubation with high-density lipoprotein.

Keywords: Propofol, cholesterol efflux, reactive oxygen species, inflammation, high-density lipoprotein, rat aortic endothelial cells

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Hsu CP, Lin CH, Kuo CY. Endothelial-cell inflammation and damage by reactive oxygen species are prevented by propofol via ABCA1-mediated cholesterol efflux. Int J Med Sci 2018; 15(10):978-985. doi:10.7150/ijms.24659. Available from http://www.medsci.org/v15p0978.htm