Abstract
Possible anti-atherogenic activities of emodin were found. In this study, we investigated the effects of emodin on monocyte chemotactic protein (MCP)-1 and tissue inhibitor of metalloproteinases (TIMP)-2 secretion using aortic smooth muscle cell A-10. Both of them are considered to play important roles in the pathogenesis of atherosclerosis. Emodin had a dose-dependent inhibitory effect on tumor necrosis factor-αinduced MCP-1 secretion. Exposure to 50 and 100 μM emodin caused significant inhibition of TIMP-2 secretion. These results suggested that emodin has an anti-atherogenic potential. Also, the estrogenic activity of emodin was investigated. Emodin competed against estrogen in estrogen receptor (ER) binding, indicating that emodin is an estrogenic mycotoxin. Seeing that estrogens also inhibit the secretion of MCP-1, ER(s) may be a mediator of the emodin′s transducing signal.
