Oxidized low-density lipoprotein (ox-LDL) was known to induce endothelial cell injury to the progression of atherosclerosis (AS). Sophocarpine (SPC), a compound of sophora alkaloids isolated from the plant Sophora alopecuroides, has been shown to exhibit various pharmacological activities. This study was designed to investigate the protective effect of SPC on ox-LDL-induced endothelial cells and explored its underlying mechanism. Our results show that SPC pre-incubation ameliorated ox-LDL-mediated HAECs cytotoxicity, DNA fragmentation, and apoptosis in a dose-dependent manner. Moreover, SPC significantly downregulated the mRNA or protein expression level of pro-inflammatory mediators (TGF-β, IL-6, IL-1β, TNF-α) and pro-inflammatory vascular adhesion molecules (VCAM-1, ICAM-1, and E-selectin). Mechanistically, SPC pre-treatment downregulated IκBα expression and inhibited translocation of NF-κB in ox-LDL-mediated HAECs, overexpression of NF-κB p65 counteracted the cytoprotective and anti-apoptotic effect of SPC, suggesting that its action is dependent on NF-κB signaling pathway. Collectively, SPC suppresses ox-LDL-induced HAECs injury by inhibiting the NF-κB signaling pathway.

已知氧化型低密度脂蛋白（ox-LDL）诱导内皮细胞损伤，导致动脉粥样硬化（AS）的发展。Sophocarpine（SPC）是从植物Sophora alopecuroides分离得到的槐属生物碱的化合物，已显示出多种药理活性。本研究旨在研究SPC对ox-LDL诱导的内皮细胞的保护作用，并探讨其潜在机制。我们的结果表明，SPC预温育以剂量依赖的方式改善了ox-LDL介导的HAEC的细胞毒性，DNA片段化和凋亡。此外，SPC显着下调促炎性介质（TGF-β，IL-6，IL-1β，TNF-α）和促炎性血管黏附分子（VCAM-1，ICAM-1和E-选择素）。机械上，SPC预处理下调了ox-LDL介导的HAEC中IκBα的表达并抑制了NF-κB的转运，NF-κBp65的过表达抵消了SPC的细胞保护和抗凋亡作用，表明其作用依赖于NF-κB信号传导途径。总体而言，SPC通过抑制NF-κB信号通路来抑制ox-LDL诱导的HAECs损伤。