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天然黄酮 tricetin 通过抑制 Egr-1 抑制氧化型 LDL 诱导的内皮炎症。

Natural flavone tricetin suppresses oxidized LDL-induced endothelial inflammation mediated by Egr-1.

机构信息

Department of Cardiovascular Medicine, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, PR China.

Department of Central Laboratory, Jingjiang People's Hospital, Jingjiang, Jiangsu 214500, PR China.

出版信息

Int Immunopharmacol. 2020 Mar;80:106224. doi: 10.1016/j.intimp.2020.106224. Epub 2020 Jan 25.

DOI:10.1016/j.intimp.2020.106224
PMID:31991371
Abstract

Atherosclerosis is the primary cause of many cardiovascular diseases. Endothelial dysfunction is recognized as a crucial early event in atherosclerotic lesion formation. Tricetin is a natural flavonoid derivative that has demonstrated a wide range of therapeutic properties. This study investigates the protective effect of tricetin in cultured endothelial cells. The results of our study show that tricetin suppressed oxidized low-density lipoprotein (ox-LDL)-induced expression of pro-inflammatory monocyte chemotactic protein-1 (MCP-1) and interleukin-1β (IL-1β), as well as the generation of reactive oxygen species (ROS). Furthermore, our findings indicate that tricetin suppressed ox-LDL-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). At the cellular level, the presence of tricetin inhibited ox-LDL-induced monocyte adhesion to endothelial cells. Mechanistically, we showed that tricetin suppressed the induction of the endothelial receptor for ox-LDL, lectin-like ox-LDL receptor-1 (LOX-1), and the transcriptional factor early growth response 1 (Egr-1) as well as extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) activation. These data demonstrate that tricetin is a natural protective agent in vascular endothelial cells, indicating that tricetin could have a potentially beneficial effect in the modulation of atherosclerosis.

摘要

动脉粥样硬化是许多心血管疾病的主要原因。内皮功能障碍被认为是动脉粥样硬化病变形成的一个关键早期事件。三羟黄酮是一种天然黄酮类衍生物,具有广泛的治疗特性。本研究探讨了三羟黄酮在培养的内皮细胞中的保护作用。我们的研究结果表明,三羟黄酮抑制了氧化型低密度脂蛋白(ox-LDL)诱导的促炎单核细胞趋化蛋白-1(MCP-1)和白细胞介素-1β(IL-1β)的表达,以及活性氧(ROS)的产生。此外,我们的研究结果表明,三羟黄酮抑制了 ox-LDL 诱导的细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)的表达。在细胞水平上,三羟黄酮抑制了 ox-LDL 诱导的单核细胞黏附到内皮细胞上。在机制上,我们表明三羟黄酮抑制了 ox-LDL 内皮受体凝集素样 ox-LDL 受体-1(LOX-1)和转录因子早期生长反应 1(Egr-1)的诱导,以及细胞外信号调节蛋白激酶 1 和 2(ERK1/2)的激活。这些数据表明,三羟黄酮是血管内皮细胞中的一种天然保护剂,表明三羟黄酮可能在调节动脉粥样硬化方面具有潜在的有益作用。

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