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22 March 2019 : Laboratory Research  

Astragaloside IV Protects Against Oxidized Low-Density Lipoprotein (ox-LDL)-Induced Endothelial Cell Injury by Reducing Oxidative Stress and Inflammation

Zhongsheng Zhu1AEG*, Jinyu Li1BC, Xiaorong Zhang1B

DOI: 10.12659/MSM.912894

Med Sci Monit 2019; 25:2132-2140

Abstract

BACKGROUND: Endothelial injury is the main mechanism of atherosclerosis, and is caused by oxidized low-density lipoprotein (ox-LDL). Astragaloside IV (AS-IV) is the primary active ingredient of the Chinese herb Huangqi, and exhibits antioxidant and anti-inflammatory properties in cardiovascular diseases. This study investigated the protective effect of AS-IV in human umbilical vein endothelial cells (HUVECs).

MATERIAL AND METHODS: HUVEC cells were induced with ox-LDL to establish an in vitro atherosclerosis model. Then HUVECs were pretreated for 1 h with AS-IV at different concentrations (10, 20, and 50 μM) and then exposed to ox-LDL (100 μg/mL) for 48 h. The cell viability, lactate dehydrogenase (LDH) release, apoptosis, migration, intracellular reactive oxygen species (ROS), and NADPH oxidase activity of HUVECs were measured. qRT-PCR was performed to measure the mRNA expressions of Nrf2, HO-1, TNFα, and IL-6. Enzyme-linked immunosorbent assay (ELISA) was performed to measure the supernatant contents of TNFα and IL-6.

RESULTS: Exposure of HUVECs to ox-LDL reduced cell viability and migration, induced apoptosis, and increased intracellular ROS production and NADPH oxidase. Pretreatment with AS-IV (10, 20, and 50 μM) significantly enhanced the cell viability and migration, suppressed LDH release, apoptosis, ROS production, and NADPH oxidase in HUVECs, in a concentration-dependent manner. The AS-IV (50 μM) alone did not show significant differences from control. AS-IV increased mRNA expressions of Nrf2 and HO-1 and decreased mRNA expressions of TNFα and IL-6 in the ox-LDL-HUEVC cells. Furthermore, AS-IV reduced supernatant contents of TNFα and IL-6.

CONCLUSIONS: Astragaloside IV prevents ox-LDL-induced endothelial cell injury by reducing apoptosis, oxidative stress, and inflammatory response.

Keywords: atherosclerosis, endothelial cells, Oxidative Stress, Receptors, Oxidized LDL, Antioxidants, Apoptosis, Cell Survival, Human Umbilical Vein Endothelial Cells, L-Lactate Dehydrogenase, Lipoproteins, LDL, NADP, NADPH Oxidases, Protective Agents, Reactive Oxygen Species, Saponins, Triterpenes

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750