PMID- 31656544 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20201001 IS - 1792-0981 (Print) IS - 1792-1015 (Electronic) IS - 1792-0981 (Linking) VI - 18 IP - 5 DP - 2019 Nov TI - Salidroside prevents tumor necrosis factor-alpha-induced vascular inflammation by blocking mitogen-activated protein kinase and NF-kappaB signaling activation. PG - 4137-4143 LID - 10.3892/etm.2019.8064 [doi] AB - 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)-alpha-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 microM. Additionally, salidroside decreased the expression levels of the cell adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) in TNF-alpha-stimulated CMECs, thus suppressing monocyte-to-CMEC adhesion. Salidroside also decreased the production of inflammatory cytokines such as interleukin (IL)-1beta, IL-6 and monocyte chemotactic protein 1 (MCP-1) in TNF-alpha-induced CMECs, as well as suppressing TNF-alpha-activated mitogen-activated protein kinase (MAPK) and NF-kappaB activation. Since MAPKs and NF-kappaB both serve notable roles in regulating the expression of VCAM-1, IL-1beta, 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-kappaB activation in TNF-alpha-induced CMECs. These results indicated that salidroside may have potential applications as a therapeutic agent against vascular inflammation and atherosclerosis. CI - Copyright (c) 2019, Spandidos Publications. FAU - Li, Ruoshui AU - Li R AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Dong, Zhen AU - Dong Z AD - Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China. FAU - Zhuang, Xinyu AU - Zhuang X AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Liu, Rongchen AU - Liu R AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Yan, Fangying AU - Yan F AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Chen, Yufei AU - Chen Y AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Gao, Xiufang AU - Gao X AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. FAU - Shi, Haiming AU - Shi H AD - Department of Cardiology, Huashan Hospital, Fudan University, Shanghai 200036, P.R. China. LA - eng PT - Journal Article DEP - 20190927 PL - Greece TA - Exp Ther Med JT - Experimental and therapeutic medicine JID - 101531947 PMC - PMC6812474 OTO - NOTNLM OT - endothelial cells OT - monocyte adhesion OT - salidroside OT - tumor necrosis factor-alpha OT - vascular inflammation EDAT- 2019/10/28 06:00 MHDA- 2019/10/28 06:01 PMCR- 2019/09/27 CRDT- 2019/10/29 06:00 PHST- 2019/03/07 00:00 [received] PHST- 2019/09/10 00:00 [accepted] PHST- 2019/10/29 06:00 [entrez] PHST- 2019/10/28 06:00 [pubmed] PHST- 2019/10/28 06:01 [medline] PHST- 2019/09/27 00:00 [pmc-release] AID - ETM-0-0-8064 [pii] AID - 10.3892/etm.2019.8064 [doi] PST - ppublish SO - Exp Ther Med. 2019 Nov;18(5):4137-4143. doi: 10.3892/etm.2019.8064. Epub 2019 Sep 27.