Salidroside prevents tumor necrosis factor‑α‑induced vascular inflammation by blocking mitogen‑activated protein kinase and NF‑κB signaling activation

Li,Ruoshui; Dong,Zhen; Zhuang,Xinyu; Liu,Rongchen; Yan,Fangying; Chen,Yufei; Gao,Xiufang; Shi,Haiming

doi:10.3892/etm.2019.8064

Salidroside prevents tumor necrosis factor‑α‑induced vascular inflammation by blocking mitogen‑activated protein kinase and NF‑κB signaling activation

Authors:
- Ruoshui Li
- Zhen Dong
- Xinyu Zhuang
- Rongchen Liu
- Fangying Yan
- Yufei Chen
- Xiufang Gao
- Haiming Shi
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Affiliations: Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China, Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China
Published online on: September 27, 2019 https://doi.org/10.3892/etm.2019.8064
Pages: 4137-4143
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Vascular inflammation is a key factor in the pathogenesis of atherosclerosis. Salidroside is an important active ingredient extracted from the root of the Rhodiola rosea plant, which has been reported to have antioxidative, anti‑cancer, neuroprotective and cardioprotective effects. However, the effects of salidroside on vascular inflammation have not been clarified. The purpose of the present study was to investigate the protective effects of salidroside against tumor necrosis factor (TNF)‑α‑induced vascular inflammation in cardiac microvascular endothelial cells (CMECs), a specific cell type derived from coronary micro‑vessels. Over a 24‑h period, salidroside did not exert any significant cytotoxicity up to a dose of 100 µM. Additionally, salidroside decreased the expression levels of the cell adhesion molecule vascular cell adhesion molecule‑1 (VCAM‑1) in TNF‑α‑stimulated CMECs, thus suppressing monocyte‑to‑CMEC adhesion. Salidroside also decreased the production of inflammatory cytokines such as interleukin (IL)‑1β, IL‑6 and monocyte chemotactic protein 1 (MCP‑1) in TNF‑α‑induced CMECs, as well as suppressing TNF‑α‑activated mitogen‑activated protein kinase (MAPK) and NF‑κB activation. Since MAPKs and NF‑κB both serve notable roles in regulating the expression of VCAM‑1, IL‑1β, IL‑6 and MCP‑1, the present study provided a preliminary understanding of the mechanism underlying the protective effects of salidroside. Overall, salidroside alleviated vascular inflammation by mediating MAPK and NF‑κB activation in TNF‑α‑induced CMECs. These results indicated that salidroside may have potential applications as a therapeutic agent against vascular inflammation and atherosclerosis.

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