Protective effects of tanshinone ⅡA on endothelial progenitor cells injured by tumor necrosis factor‑α

Wang,Xing‑Xiang; Yang,Jin‑Xiu; Pan,Yan‑Yun; Zhang,Ye‑Fei

doi:10.3892/mmr.2015.3969

Protective effects of tanshinone ⅡA on endothelial progenitor cells injured by tumor necrosis factor‑α

Authors:
- Xing‑Xiang Wang
- Jin‑Xiu Yang
- Yan‑Yun Pan
- Ye‑Fei Zhang
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Affiliations: Department of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China, Department of Cardiology, The First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310006, P.R. China, Department of Emergency, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China
Published online on: June 22, 2015 https://doi.org/10.3892/mmr.2015.3969
Pages: 4055-4062
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Tanshinone ⅡA (Tan ⅡA) is a Traditional Chinese Medicine commonly used in Asian and Western countries for the prevention and treatment of cardiovascular disorders, such as atherosclerosis. Endothelial dysfunction and associated inflammatory processes have a critical role in the development of atherosclerosis. Endothelial progenitor cells (EPCs) have been demonstrated to be involved in certain aspects of the endothelial repair process. The present study aimed to investigate the putative protective effects of Tan ⅡA on EPCs injured by tumor necrosis factor‑α (TNF‑α). The potential effects of Tan ⅡA on TNF-α-stimulated EPC proliferation, migration, adhesion, in vitro tube formation ability and paracrine activity were investigated in the current study. The results indicated that TNF‑α impaired EPC proliferation, migration, adhesion capacity and vasculogenesis ability in vitro as well as promoted EPC secretion of inflammatory cytokines, including monocyte chemoattractant protein‑1 (MCP‑1), interleukin‑6 (IL‑6) and soluble CD40 ligand (sCD40L). However, Tan ⅡA was able to reverse these effects. In conclusion, these findings demonstrated that Tan ⅡA may have the potential to protect EPCs against damage induced by TNF‑α. Therefore, these results may provide evidence for the pharmacological basis of Tan ⅡA and its potential use in the prevention and treatment of early atherosclerosis associated with EPC and endothelial damage.

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