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Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling

Oxidative injury of vascular endothelial cells in the initial event of atherosclerosis (AS) in diabetes was assessed in the present study. The antioxidant effect of oleanolic acid (OA) has attracted much attention. In the present study the potential effects of OA on human umbilical vein endothelial...

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Autores principales: Zhang, Wei, Feng, Jian, Cheng, Biao, Lu, Qing, Chen, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131357/
https://www.ncbi.nlm.nih.gov/pubmed/30106101
http://dx.doi.org/10.3892/mmr.2018.9354
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author Zhang, Wei
Feng, Jian
Cheng, Biao
Lu, Qing
Chen, Xiaoping
author_facet Zhang, Wei
Feng, Jian
Cheng, Biao
Lu, Qing
Chen, Xiaoping
author_sort Zhang, Wei
collection PubMed
description Oxidative injury of vascular endothelial cells in the initial event of atherosclerosis (AS) in diabetes was assessed in the present study. The antioxidant effect of oleanolic acid (OA) has attracted much attention. In the present study the potential effects of OA on human umbilical vein endothelial cells (HUVECs) were investigated. Cell viability was examined using the CCK-8 assay. The activity of oxidative stress parameters was determined using commercial kits. Flow cytometry analysis was performed to detect the level of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cell apoptosis. The expression levels of target genes and proteins were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. It was indicated that cell viability that was suppressed by high glucose was increased by the pretreatment of OA, and nitric oxide (NO) generation, the activities of superoxide dismutase (SOD) and catalase (CAT) were recovered by OA. By contrast, it was observed that OA decreased the MDA content. Notably, the pretreatment of OA alleviated mitochondria damage by reducing the level of ROS and maintaining MMP. In addition, apoptosis that was caused by high glucose was reduced by OA. Pro-apoptotic genes (caspase-3, Fas, Fasl) and anti-apoptotic gene (Bcl-2) expression levels were decreased and increased in the OA groups, respectively. Furthermore, the activity of AKT/endothelial nitric oxide synthase (eNOS) signaling was elevated by OA. Taken together, it was suggested that OA could protect against oxidative stress-induced apoptosis of HUVECs, which was associated with AKT/eNOS signaling pathway.
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spelling pubmed-61313572018-09-14 Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling Zhang, Wei Feng, Jian Cheng, Biao Lu, Qing Chen, Xiaoping Mol Med Rep Articles Oxidative injury of vascular endothelial cells in the initial event of atherosclerosis (AS) in diabetes was assessed in the present study. The antioxidant effect of oleanolic acid (OA) has attracted much attention. In the present study the potential effects of OA on human umbilical vein endothelial cells (HUVECs) were investigated. Cell viability was examined using the CCK-8 assay. The activity of oxidative stress parameters was determined using commercial kits. Flow cytometry analysis was performed to detect the level of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cell apoptosis. The expression levels of target genes and proteins were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. It was indicated that cell viability that was suppressed by high glucose was increased by the pretreatment of OA, and nitric oxide (NO) generation, the activities of superoxide dismutase (SOD) and catalase (CAT) were recovered by OA. By contrast, it was observed that OA decreased the MDA content. Notably, the pretreatment of OA alleviated mitochondria damage by reducing the level of ROS and maintaining MMP. In addition, apoptosis that was caused by high glucose was reduced by OA. Pro-apoptotic genes (caspase-3, Fas, Fasl) and anti-apoptotic gene (Bcl-2) expression levels were decreased and increased in the OA groups, respectively. Furthermore, the activity of AKT/endothelial nitric oxide synthase (eNOS) signaling was elevated by OA. Taken together, it was suggested that OA could protect against oxidative stress-induced apoptosis of HUVECs, which was associated with AKT/eNOS signaling pathway. D.A. Spandidos 2018-10 2018-08-03 /pmc/articles/PMC6131357/ /pubmed/30106101 http://dx.doi.org/10.3892/mmr.2018.9354 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhang, Wei
Feng, Jian
Cheng, Biao
Lu, Qing
Chen, Xiaoping
Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title_full Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title_fullStr Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title_full_unstemmed Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title_short Oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating AKT/eNOS signaling
title_sort oleanolic acid protects against oxidative stress-induced human umbilical vein endothelial cell injury by activating akt/enos signaling
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131357/
https://www.ncbi.nlm.nih.gov/pubmed/30106101
http://dx.doi.org/10.3892/mmr.2018.9354
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