Escin ameliorates inflammation via inhibiting mechanical stretch and chemically induced Piezo1 activation in vascular endothelial cells

被引:8
|
作者
Wang, Yuman [1 ]
Chu, Tianjiao [1 ]
Pan, Xianmei [2 ,3 ]
Bian, Yifei [1 ,4 ]
Li, Jing [1 ,2 ,3 ,4 ]
机构
[1] Shandong Univ Tradit Chinese Med, Innovat Res Inst Tradit Chinese Med, Jinan, Shandong, Peoples R China
[2] Guangzhou Univ Chinese Med, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China
[3] Guangzhou Univ Chinese Med, Lingnan Med Res Ctr, Guangzhou, Guangdong, Peoples R China
[4] Shandong Univ Tradit Chinese Med, Innovat Res Inst Tradit Chinese Med, 4655 Daxue Rd, Jinan 250355, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Escin; Piezo1; Mechanical stretch; Inflammation; Endothelial cells; NF-KAPPA-B; LPS-INDUCED INFLAMMATION; ANTHRACYCLINE CHEMOTHERAPY; SIGNALING PATHWAYS; ION CHANNELS; INTERLEUKIN-1-BETA; THROMBOPHLEBITIS; ARCHITECTURE; PRESSURE; HYPOXIA;
D O I
10.1016/j.ejphar.2023.175951
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Escin is an active ingredient used in the treatment of phlebitis. However, the pharmacological mechanism of escin remains largely unclear. Here, we aimed to determine the molecular basis for the therapeutic effect of escin. Human umbilical vein endothelial cells (HUVECs) were subjected to shear-stress assays with or without escin. Intracellular Ca2+ levels, inflammatory factors and the activity of NF-& kappa;B were measured in endothelial cells (ECs) after mechanical-stretch or Yoda1 activation. Isometric tensions in aortic rings were identified. In addition, murine liver endothelial cells (MLECs) isolated from Piezo1 endothelial specific knockout mice (Piezo1o EC) were used to explore the role of Piezo1. Our results showed that escin inhibited inflammatory factors, intracellular Ca2+ levels and Yoda1-evoked relaxation of thoracic aorta rings. Cell alignment induced by shear stress was inhibited by escin in HUVECs, and Piezo1 siRNA was used to show that this effect was dependent on Piezo1 channels. Moreover, escin reduced the inflammation and inhibited the activity of NF-& kappa;B in ECs with mechanical -stretch, which were insensitive to Piezo1 deletion. SN50, an NF-& kappa;B antagonist, significantly inhibited the me-chanical stretch-induced inflammatory response. In addition, escin reduced inflammation in ECs subjected to mechanical-stretch, which was insensitive after using NF-& kappa;B antagonist. Collectively, our results demonstrate that escin inhibits the mechanical stretch-induced inflammatory response via a Piezo1-mediated NF-& kappa;B pathway. This study improves our understanding of a molecular target of escin that mediates its effect on chronic vascular inflammation.
引用
收藏
页数:12
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