Inflammation is a key regulator in the progression of atherosclerosis (AS) which extremely affects people’s health. Secoisolariciresinol diglucoside (SDG), a plant lignan, is relevant to angiogenesis and cardioprotection against ischemia-reperfusion injury and improves vascular disorders. However, the effect of SDG on cardiovascular disorder is not clear. In the present study, we aimed to investigate the effects of SDG on lipopolysaccharide- (LPS-) stimulated Human Umbilical Vein Endothelial Cells (HUVECs) and elucidate the underlying mechanism. The LPS-stimulated HUVEC cellular model was established. The cell viability, the cell tube formation activity, the nitric oxide (NO) release, the levels of inflammatory cytokine interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), the activation of nuclear factor kappa-B (NF-κB) pathway, and the expression of protein kinase B (Akt) were determined using Cell Counting Kit-8, cell tube-formation assay, western blotting, and enzyme-linked immunosorbent assay. Our results revealed that SDG reduces the angiogenic capacity of HUVECs and inhibited LPS-mediated HUVEC injury and apoptosis. In addition, SDG increased NO release and decreased the levels of IL-1β, IL-6, and TNF-α in LPS-treated HUVECs. Meanwhile, SDG inhibited the NF-κB pathway and downregulated Akt expression in LPS-induced HUVECs. Our results indicated that SDG relieves LPS-mediated HUVEC injury by inhibiting the NF-κB pathway which is partly dependent on the disruption of Akt activation. Therefore, SDG exerts its cytoprotective effects in the context of LPS-treated HUVECs via regulation of the Akt/IκB/NF-κB pathway and may be a potential treatment drug for cardiovascular disease.

中文翻译：

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Secoisolariciresinol Diglucoside 通过抑制人脐静脉内皮细胞的 Akt/IκB/NF-κB 通路发挥抗炎和抗凋亡作用。

炎症是动脉粥样硬化（AS）进展的关键调节因素，严重影响人们的健康。Secoisolariciresinol diglucoside (SDG) 是一种植物木脂素，与血管生成和针对缺血再灌注损伤的心脏保护作用有关，并可改善血管疾病。然而，SDG 对心血管疾病的影响尚不清楚。在本研究中，我们旨在研究SDG对脂多糖（LPS）刺激的人脐静脉内皮细胞（HUVEC）的影响并阐明其潜在机制。建立了LPS刺激的HUVEC细胞模型。细胞活力、细胞管形成活性、一氧化氮（NO）释放、炎症细胞因子白细胞介素-1β （ IL- 1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF）水平- α )、核因子 kappa-B (NF- κ B) 通路的激活以及蛋白激酶 B (Akt) 的表达使用 Cell Counting Kit-8、细胞管形成测定、蛋白质印迹和酶测定连锁免疫吸附测定。我们的结果表明，SDG 降低了 HUVEC 的血管生成能力，并抑制 LPS 介导的 HUVEC 损伤和凋亡。此外，SDG 增加了LPS 处理的 HUVEC 中NO 的释放，并降低了 IL-1 β、IL-6 和 TNF- α的水平。同时，SDG 抑制 NF- κ B 通路并下调 LPS 诱导的 HUVEC 中 Akt 的表达。我们的结果表明，SDG 通过抑制 NF- κ B 途径减轻 LPS 介导的 HUVEC 损伤，该途径部分依赖于 Akt 激活的破坏。因此，SDG 通过调节 Akt/ IκB /NF -κB通路在 LPS 处理的 HUVEC 中发挥细胞保护作用，可能成为心血管疾病的潜在治疗药物。