Brazilian Green Propolis Inhibits Ox-LDL-Stimulated Oxidative Stress in Human Umbilical Vein Endothelial Cells Partly through PI3K/Akt/mTOR-Mediated Nrf2/HO-1 Pathway

Wenwen Yuan,Shiqiang Wang,Hongzhuan Xuan,Xinying Liu,Huasong Chang,Hui Liu

doi:10.1155/2019/5789574

Abstract

Propolis has been widely used as a dietary supplement for its health benefits, including cardiovascular protective effects. The aim of this study was to investigate the cytoprotective effects of Brazilian green propolis (BP) against oxidized low-density lipoprotein (Ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage. Our results suggested that treatment with BP rescued Ox-LDL-stimulated HUVECs cell viability losses, which might be associated with its inhibitive effects on the cell apoptosis and autophagy. We also noticed that BP restored Ox-LDL-stimulated HUVECs oxidative stress, by induced antioxidant gene expressions, including Heme oxygenase-1 and its upstream mediator, Nrf2, which were mediated by the activation of the phosphorylation of PI3K/Akt/mTOR. Pretreatment with wortmannin, PI3K/AKT inhibitor, abolished BP induced Nrf2 nuclear translocation and HO-1 level. Our results demonstrated that BP protected HUVECs against oxidative damage partly via PI3K/Akt/mTOR-mediated Nrf/HO-1 pathway, which might be applied into preventing Ox-LDL mediated cardiovascular diseases.

Highlights

Atherosclerosis is a complex chronic inflammatory and metabolic disease, which is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted leading to lipid and protein oxidation in the vascular wall
Our previous study showed that poplar propolis could protect human umbilical vein endothelial cells (HUVECs) induced by Oxidized low-density lipoprotein (Ox-LDL), and here we further demonstrated that Brazilian green propolis (1.25, 2.5, and 5 μg/mL) could improve cell viability in Ox-LDL-treated HUVECs at
To further determine the antioxidant mechanism of extracted Brazilian green propolis (EEBP) depressing oxidative stress induced by Ox-LDL, we investigated the effects of EEBP treatment on PI3K/Akt/mTOR signaling pathway

Summary

Introduction

Atherosclerosis is a complex chronic inflammatory and metabolic disease, which is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted leading to lipid and protein oxidation in the vascular wall. Accumulation of lipoproteins in the vessel wall provides the initial trigger for vascular inflammation, causing endothelial dysfunction and monocyte recruitment [1]. Oxidized low-density lipoprotein (Ox-LDL) is a crucial factor in triggering the development of atherosclerosis [2]. It directly targets vascular endothelial cells (VECs) to induce endothelium injury or dysfunction, but can activate monocytes and macrophages by binding to scavenger receptors leading to the formation of plaque and secretion of proinflammatory cytokines [3, 4]. Protecting the endothelial cells against damage or death has been considered a novel target for the atherosclerotic treatment A mounting evidence indicated that endothelial cells dysfunctions may be harmful to the plaque vulnerability [5, 6].

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