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薯蓣皂苷通过NF-κB途径抑制TNF-α诱导的VCAM-1、ICAM-1和EL表达介导的强效抗炎作用。

Potent anti-inflammatory effect of dioscin mediated by suppression of TNF-α-induced VCAM-1, ICAM-1and EL expression via the NF-κB pathway.

作者信息

Wu Shan, Xu Hui, Peng Jinyong, Wang Changyuan, Jin Yue, Liu Kexin, Sun Huijun, Qin Jianhua

机构信息

Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 west section, Lvshun South Road, Lvshunkou District, Dalian 116044, Liaoning Province, China.

Department of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Shahekou District, Dalian 116023, Liaoning Province, China.

出版信息

Biochimie. 2015 Mar;110:62-72. doi: 10.1016/j.biochi.2014.12.022. Epub 2015 Jan 9.

DOI:10.1016/j.biochi.2014.12.022
PMID:25577996
Abstract

The modulation of adhesion molecule expression and the reduction of aberrant leukocyte adhesion to the endothelium are attractive approaches for treating inflammation-related vascular complications, including atherosclerosis. Dioscin has a variety of biological activities including anti-inflammatory activity. However, the molecular mechanisms behind dioscin's anti-inflammatory effects are not fully understood. In this study, we investigated the molecular mechanism involved in the effects of dioscin on inflammatory mediators in tumor necrosis factor-α (TNF-α)-stimulated human umbilical vein endothelial cells (HUVECs). In vitro, dioscin decreased monocyte adhesion to TNF-α-treated HUVECs by reducing vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression and inhibiting endothelial lipase (EL) expression in TNF-α-treated HUVECs and macrophages by blocking the nuclear factor-κB (NF-κB) pathway. Thus, dioscin might inhibit inflammation by interrupting the NF-κB signaling pathway and could potentially contribute to treatments for inflammatory diseases and atherosclerosis.

摘要

调节黏附分子表达以及减少异常白细胞与内皮的黏附是治疗包括动脉粥样硬化在内的炎症相关血管并发症的有吸引力的方法。薯蓣皂苷具有多种生物活性,包括抗炎活性。然而,薯蓣皂苷抗炎作用背后的分子机制尚未完全明确。在本研究中,我们调查了薯蓣皂苷对肿瘤坏死因子-α(TNF-α)刺激的人脐静脉内皮细胞(HUVECs)中炎症介质作用的分子机制。在体外,薯蓣皂苷通过降低血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子1(ICAM-1)的表达,以及通过阻断核因子-κB(NF-κB)途径抑制TNF-α处理的HUVECs和巨噬细胞中内皮脂肪酶(EL)的表达,从而减少单核细胞与TNF-α处理的HUVECs的黏附。因此,薯蓣皂苷可能通过中断NF-κB信号通路来抑制炎症,并可能有助于治疗炎症性疾病和动脉粥样硬化。

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