XIA Xiaodong, Ph.D.

　　College of Economic and Management, Northwest A&F University

　　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 anti-oxidative properties. This study aims to investigate the protective effect of urolithin A on ox-LDL induced endothelial dysfunction and possible modes of action. Human artery endothelial cells were incubated with 50 μg/mL ox-LDL and various concentrations of urolithin A for 24 h. Urolithin A improved the productions of NO and eNOS in a dose-dependent manner. Urolithin A markedly reduced the expressions of ICAM-1 and MCP-1 and further attenuated THP-1 cell adhesion. In addition, urolithin A suppressed expressions of TNF-α, IL-6 and ET-1, and increased PPAR-γ mRNA expression. Moreover, urolithin A decreased miR-27 expression, and overexpression of miR-27 by adding pre-miR-27 abolished the ability of urolithin A to improve ox-LDL induced PPAR-γ decrease. Furthermore, urolithin A significantly down-regulated phosphorylated ERK1/2 while decreasing IL-6 level and elevating PPAR-γ. These findings suggest that urolithin A could alleviate endothelial dysfunction induced by ox-LDL partially through modulating miR-27 expression and ERK/PPAR-γ pathway.