Zhang Jiacheng, Wang Nan, Xin Tianyou, Zhu Xiaojun, Lang Shengkun, Ge Xin
Department of Emergency and Critical Care Medicine, Wuxi 9th People's Hospital Affiliated to Soochow University, Liangxi Road 999, Wuxi, Jiangsu, 214000, People's Republic of China.
Department of Ultrasound, Wuxi 9th People's Hospital Affiliated to Soochow University, Wuxi, Jiangsu, People's Republic of China.
Thromb J. 2025 May 20;23(1):51. doi: 10.1186/s12959-025-00739-3.
Lower extremity deep vein thrombosis (LEDVT) is a common vascular disease, with its pathogenesis mainly involving inflammatory responses and oxidative stress. Liquiritin (LIQ) is a flavonoid that exhibits pharmacological effects such as anti-inflammatory and antioxidant properties. This study aimed to investigate the role of LIQ in LEDVT and its potential mechanisms.
We established an LEDVT model in mice by ligating the inferior vena cava (IVC) and performed in vitro experiments by stimulating human umbilical vein endothelial cells (HUVECs) with IL-1β (10 ng/mL) to simulate endothelial cell injury.
We found that LIQ significantly reduced the size and weight of thrombi and decreased the concentrations of inflammatory factors TNF-α and IL-6 in the IVC of LEDVT mice. Furthermore, LIQ inhibited the secretion of prothrombotic mediators such as tissue factor (TF) and vascular cell adhesion molecule-1 (VCAM-1). Administration of LIQ resulted in a notable reduction in immune inflammatory cells in the IVC of LEDVT mice. LIQ also demonstrated antioxidant properties, as the treatment of LIQ enhanced SOD activity and restored ROS levels to normal in the IVC. Similarly, LIQ reduced the formation of inflammatory factors and the secretion of prothrombotic mediators by HUVECs while inhibiting oxidative stress in HUVECs. Finally, LIQ effectively suppressed the levels of phosphorylated p65 in both the IVC and HUVECs.
LIQ reduces inflammatory responses and oxidative stress in LEDVT by inhibiting the NF-κB signaling pathway. This finding provides new insights into the prevention and treatment of LEDVT.
下肢深静脉血栓形成（LEDVT）是一种常见的血管疾病，其发病机制主要涉及炎症反应和氧化应激。甘草苷（LIQ）是一种黄酮类化合物，具有抗炎和抗氧化等药理作用。本研究旨在探讨LIQ在LEDVT中的作用及其潜在机制。
通过结扎下腔静脉（IVC）建立小鼠LEDVT模型，并通过用IL-1β（10 ng/mL）刺激人脐静脉内皮细胞（HUVECs）进行体外实验，以模拟内皮细胞损伤。
我们发现LIQ显著减小了LEDVT小鼠IVC中血栓的大小和重量，并降低了炎症因子TNF-α和IL-6的浓度。此外，LIQ抑制了组织因子（TF）和血管细胞黏附分子-1（VCAM-1）等促血栓形成介质的分泌。给予LIQ导致LEDVT小鼠IVC中免疫炎症细胞显著减少。LIQ还表现出抗氧化特性，因为LIQ处理增强了IVC中的超氧化物歧化酶（SOD）活性并将活性氧（ROS）水平恢复正常。同样，LIQ减少了HUVECs中炎症因子的形成和促血栓形成介质的分泌，同时抑制了HUVECs中的氧化应激。最后，LIQ有效抑制了IVC和HUVECs中磷酸化p65的水平。
LIQ通过抑制NF-κB信号通路降低LEDVT中的炎症反应和氧化应激。这一发现为LEDVT的预防和治疗提供了新的见解。
