Emodin and rhein inhibit LIGHT-induced monocytes migration by blocking of ROS production

LIGHT is known to act as a novel mediator for atherogenesis. Furthermore, it has been reported that emodin, an active component extracted from rhubarb, can stop the growth of cancer cells. However, it is not known if emodin exerts anti-atherogenic effects in the human monocyte, THP-1, following treatment with LIGHT. In this study, we evaluated the inhibitory effect of emodin and rhein on LIGHT-induced migration in THP-1. Emodin and rhein decreased the level of LIGHT-induced generation of ROS, as well as the expression of CCR1, CCR2 and ICAM-1 and the production of IL-8, MCP-1, TNF-α, and IL-6. Emodin and rhein also decreased the phosphorylation of the p38 MAPK and IkB-α. Furthermore, the NADPH oxidase assembly inhibitor, AEBSF, and the blocker of NADPH oxidase, p47phox small interference RNA (siRNA), also efficiently blocked LIGHT-induced migration, CCR1, CCR2, ICAM-1, and HVEM expression, and p38 MAPK and NF-kB activation. These findings indicate that the inhibitory effects of emodin and rhein on LIGHT-induced migration occur via decreasing ROS production and NADPH oxidase p47phox activation. Taken together, these results indicate that emodin and rhein have the potential for use as an anti-atherosclerosis agent.

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