Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 60, Issue 9, Pages 1933-1943Publisher
WILEY
DOI: 10.1002/mnfr.201500827
Keywords
Atherosclerosis; Endothelial dysfunction; ERK signal pathway; MicroRNA-27; Urolithin A
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Funding
- New Century Excellent Talent Support Plan [NCET-13-0488]
- National Natural Science Foundation of China [31301498]
- Fundamental Research Funds in Northwest AF University [Z109021424]
- International Collaboration Partner Plan in Northwest AF University [A213021203]
- Special Fund for Sino-US Joint Research Center for Food Safety [A200021501]
- Start-up Funds for Talents in Northwest AF University [Z111021403]
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Scope: Endothelial dysfunction and inflammation are both common events occurring during the development of atherosclerosis. Previous studies have shown that urolithins, the intestinal microflora metabolites of ellagitannin, exhibit anti-inflammation and antioxidative properties. This study aims to investigate the protective effect of urolithin A (UA) on ox-LDL-induced (where ox-LDL is oxidized low-density lipoprotein) endothelial dysfunction and possible modes of action. Methods and results: Human artery endothelial cells were incubated with 50 mu g/mL ox-LDL and various concentrations of UA for 24 h. UA improved the productions of nitric oxide and endothelial nitric oxide synthase in a dose-dependent manner. UA markedly reduced the expressions of ICAM-1 (intercellular adhesion molecule 1) and MCP-1 (monocyte chemotactic protein 1) and further attenuated THP-1 (human acute monocytic leukemia cell line) cell adhesion. In addition, UA suppressed expressions of tumor necrosis factor alpha, interleukin 6, and endothelin 1, and increased PPAR-gamma (peroxisome proliferators activated receptor gamma) mRNA expression. Moreover, UA decreased miR-27 expression, and overexpression of miR-27 by adding pre-miR-27 abolished the ability of UA to improve ox-LDL-induced PPAR-gamma decrease. Furthermore, UA significantly downregulated phosphorylated ERK1/2 (where ERK is extracellular signal-regulated kinase) while decreasing interleukin 6 level and elevating PPAR-gamma. Conclusions: UA could alleviate endothelial dysfunction induced by ox-LDL partially through modulating miR-27 expression and ERK/PPAR-gamma pathway.
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