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

• Published in: Evidence-based complementary and alternative medicine Vol. 2019; no. 2019; pp. 1 - 12
• Main Authors: Liu, Hui, Wang, Shiqiang, Liu, Xinying, Chang, Huasong, Yuan, Wenwen, Xuan, Hongzhuan
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2019; Hindawi; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Antioxidants; Apoptosis; Atherosclerosis; Autophagy; Cardiovascular diseases; Cell cycle; Cell viability; Dietary supplements; Endothelial cells; Enzymes; Ethanol; Heme; Heme oxygenase (decyclizing); Immunoglobulins; Kinases; Low density lipoprotein; Natural products; Nuclear transport; Oxidation; Oxidative stress; Oxygenase; Phagocytosis; Phosphorylation; Propolis; Proteins; TOR protein; Toxicology; Translocation; Umbilical vein; Wortmannin; Brazil; China; United States > US
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2019/5789574

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.