Curcumin, a yellow pigment of turmeric in curry, has been reported to interfere with nuclear factor (NF)-κB. This study was designed to investigate the underlying pathway of the anti-inflammation effect of curcumin on endothelial cells.

Human umbilical vein endothelial cells (HUVECs) were stimulated with tumor necrosis factor (TNF)-α (10 ng/mL). The levels of intracellular reactive oxygen species (ROS) were examined using a fluorescent dye DCFH-DA, and the adhesion of U-937 monocytes to the HUVECs was then examined. Nuclear factor kappa B (NF-κB) activation was determined by the NF-κB p65 translocation to the nucleus via immunocytochemistry. The expression of the NF-κB dependent pro-inflammatory molecules were measured by RT-PCR and ELISA. The phosphorylations of c-Jun N-terminal protein kinase (JNK), p38 and STAT-3 (signal transducer and activator of transcription-3) were measured by Western blotting.

Curcumin blocked the activation of NF-κB by TNF-α, and it also reduced the ROS, monocyte adhesion and the phosphorylation of JNK, p38 and STAT-3 in the TNF-α-stimulated HUVECs. The expression of intracellular cell adhesion molecule (ICAM)-1, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8 were attenuated by curcumin at both the transcription and translation levels.

We suggest that curcumin could contribute to protection against the adverse vascular effects of the pro-inflammatory response through the modulation of NF-κB, JNK, p38 and STAT-3, and this is in addition to its antioxidant effect in endothelial cells.