Resveratrol protects late endothelial progenitor cells from TNF-α-induced inflammatory damage by upregulating Krüppel-like factor-2

Chu,Hairong; Li,Hong; Guan,Xiumei; Yan,Hong; Zhang,Xiaoyun; Cui,Xiaodong; Li,Xin; Cheng,Min

doi:10.3892/mmr.2018.8621

Resveratrol protects late endothelial progenitor cells from TNF-α-induced inflammatory damage by upregulating Krüppel-like factor-2

Authors:
- Hairong Chu
- Hong Li
- Xiumei Guan
- Hong Yan
- Xiaoyun Zhang
- Xiaodong Cui
- Xin Li
- Min Cheng
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Affiliations: Clinical Medical College, Weifang Medical University, Weifang, Shandong 261053, P.R. China
Published online on: February 20, 2018 https://doi.org/10.3892/mmr.2018.8621
Pages: 5708-5715
Copyright: © Chu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cardiovascular risk factors can negatively influence late endothelial progenitor cell (EPCs) number and functions, thus EPCs biology is a clinical implications for cardiovascular diseases. The present study aimed to investigate the potential protective effects of resveratrol (RES) on tumor necrosis factor (TNF)‑α‑induced inflammatory damage in late endothelial progenitor cells (EPCs) and to elucidate the underlying mechanisms. Late EPCs at passages 3‑5 were pretreated with RES at a concentration of 20 µmol/l for 12 h and subsequently incubated with TNF‑α (10 ng/ml) for 24 h. The adhesion, migration, proliferation and vasculogenesis of EPCs were subsequently detected. Furthermore, the mRNA expression levels of intercellular adhesion molecule‑1 (ICAM‑1) and monocyte chemoattractant protein‑1 (MCP‑1) were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Nitric oxide (NO) levels in the supernatant were determined using a colorimetric assay kit. Additionally, the mRNA and protein expression of Krüppel‑like factor‑2 (KLF2) was determined by RT‑qPCR and western blot analysis, respectively. The results indicated that TNF‑α markedly inhibited the proliferation, adhesion, migration and vasculogenesis of late EPCs. However, RES ameliorated the effects induced by TNF‑α. Furthermore, exposure of EPCs to TNF‑α decreased the levels of NO secretion and KLF2 expression at the mRNA and protein levels, but upregulated the levels of inflammatory factors, including ICAM‑1 and MCP‑1, compared with the control group. RES significantly inhibited TNF‑α‑induced inflammatory damage through upregulation of KLF2 expression and downregulation of the expression of ICAM‑1 and MCP‑1. In conclusion, RES may exert protective effects on the cardiovascular system, as demonstrated by the amelioration of TNF-α-induced inflammation in EPCs following RES treatment, and may therefore be used in the future for the prevention of cardiovascular disease.

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