Protective effects of quercetin and taraxasterol against H2O2‑induced human umbilical vein endothelial cell injury in vitro

Yang,Dongwei; Liu,Xinye; Liu,Min; Chi,Hao; Liu,Jirong; Han,Huamin

doi:10.3892/etm.2015.2713

Protective effects of quercetin and taraxasterol against H2O2‑induced human umbilical vein endothelial cell injury in vitro

Authors:
- Dongwei Yang
- Xinye Liu
- Min Liu
- Hao Chi
- Jirong Liu
- Huamin Han
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Affiliations: Department of Cardiology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan 450007, P.R. China, Department of Internal Medicine, North China Electric Power University Hospital, Beijing 102206, P.R. China
Published online on: August 25, 2015 https://doi.org/10.3892/etm.2015.2713
Pages: 1253-1260
Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Due to the association between inflammation and endothelial dysfunction in atherosclerosis, the blockage of the inflammatory process that occurs on the endothelial cells may be a useful way of preventing atherosclerosis. In the present study, human umbilical vein endothelial cells (HUVECs) were used to investigate the protective effects of quercetin and taraxasterol against H2O2‑induced oxidative damage and inflammation. HUVECs were pretreated with quercetin or taraxasterol at concentrations ranging between 0 and 210 µM for 12 h, prior to being administered different concentrations of H2O2 for 4 h. Cell viability and levels of apoptosis were assessed through cell counting kit‑8 (CCK‑8) and terminal deoxynucleotidyl transferase dUTP nick end labeling assays, respectively, to determine the injury to the HUVECs. The viability loss in the H2O2‑induced HUVECs was markedly restored in a concentration‑dependent manner by pretreatment with quercetin or taraxasterol. This effect was accompanied by significantly decreased expression of vascular cell adhesion molecule 1 (VCAM‑1) and cluster of differentiation (CD)80 for taraxasterol and that of CD80 for quercetin. In conclusion, the present study showed the protective effects of quercetin and taraxasterol against cell injury and inflammation in HUVECs and indicated that the effects were mediated via the downregulation of VCAM‑1 and CD80 expression. This study has therefore served as a preliminary investigation on the anti‑atherosclerotic and cardiovascular protective effects of quercetin and taraxasterol as dietary supplements.

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