动脉粥样硬化（AS）是常见的血管疾病，其主要影响因素是由氧化低密度脂蛋白（ox-LDL）引起的内皮损伤。作为人参的主要活性成分之一，人参皂苷Rb3具有抗炎和抗氧化作用。然而，人参皂苷Rb3在ox-LDL诱导的内皮损伤中的作用尚不清楚。本研究旨在评价人参皂苷Rb3对ox-LDL处理的人体主动脉内皮细胞（HAECs）的作用及其潜在机制。使用ox-LDL处理的HAECs建立了体外AS模型。使用细胞计数试剂盒-8（CCK-8）分析HAECs的存活率。通过流式细胞术评估凋亡。使用酶联免疫吸附法（ELISA）和西方印迹法评估氧化应激、炎症和内皮功能障碍。使用定量实时聚合酶链反应（qPCR）评估miR-513a-5p的水平。执行双荧光素酶检测法分析miR-513a-5p与一个zinc finger和BTB结构域蛋白（ZBTB20）之间的关系。HAECs暴露于ox-LDL（50μg/mL）后，降低了细胞存活率、超氧化物歧化酶（SOD）活性和内皮型一氧化氮合酶（eNOS）表达，同时增加了丙二醛（MDA）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）和可溶性细胞间黏附分子1（sICAM-1）的水平。Rb3预处理显著增强了HAECs的存活率，并降低了ox-LDL诱导的氧化应激、炎症和内皮功能障碍。ox-LDL降低了miR-513a-5p水平，而Rb3预处理逆转了这种情况。ZBTB20是HAECs中miR-513a-5p的靶点，ox-LDL上调了ZBTB20的表达，而Rb3预处理逆转了这一情况。miR-513a-5p抑制剂减弱了Rb3对ox-LDL诱导的HAECs的保护作用，而ZBTB20敲除逆转了该现象。人参皂苷Rb3通过调节miR-513a-5p/ZBTB20轴减轻了ox-LDL对HAECs的影响，这为AS的治疗提供了理论基础。

Atherosclerosis (AS) is a common vascular disease, and its main influencing factor is endothelial damage caused by oxidized low-density lipoprotein (ox-LDL). As one of the main active ingredients of ginseng, ginsenoside Rb3 has anti-inflammatory and anti-oxidative effects. However, the role of ginsenoside Rb3 in endothelial injury induced by ox-LDL is not clear.This study aimed to evaluate the effect and potential mechanism of ginsenoside Rb3 action on ox-LDL-treated human aortic endothelial cells (HAECs).The HAECs treated with ox-LDL were used to establish an in vitro AS model. The viability of the HAECs was analyzed with Cell Counting Kit-8 (CCK-8). Flow cytometry was performed to assess the apoptosis. Oxidative stress, inflammation and endothelial dysfunction were evaluated using enzyme-linked immunosorbent assay (ELISA) and western blotting. The levels of miR-513a-5p were assessed using quantitative real-time polymerase chain reaction (qPCR). A dual-luciferase assay was performed to analyze the relationship between miR-513a-5p and a zinc finger and BTB domain-containing protein (ZBTB20).Exposure of HAECs to ox-LDL (50 μg/mL) reduced cell viability, superoxide dismutase (SOD) activity and endothelial nitric oxide synthase (eNOS) expression, while increasing the levels of malondialdehyde (MDA), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), and soluble intercellular adhesion molecule-1 (sICAM-1). The pretreatment with Rb3 markedly enhanced cell viability and decreased ox-LDL-induced oxidative stress, inflammation and endothelial dysfunction in HAECs. The ox-LDL decreased the level of miR-513a-5p, which was reversed by Rb3 pretreatment. The ZBTB20 was a target of miR-513a-5p in HAECs, and ox-LDL upregulated ZBTB20 expression, which was reversed by Rb3 pretreatment. The protective effect of Rb3 on ox-LDL-induced HAECs was diminished by miR-513a-5p inhibition, which was reversed by ZBTB20 knockdown.Ginsenoside Rb3 reduces the effects of ox-LDL on HAECs by regulating the miR-513a-5p/ZBTB20 axis, which provides a theoretical basis for the treatment of AS.