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Korean Circ J. 2006 Jul;36(7):482-489. English. Original Article. https://doi.org/10.4070/kcj.2006.36.7.482
Kim YS , Ahn Y , Hong MH , Joo SY , Kim KH , Sohn IS , Park HW , Hong YJ , Kim JH , Kim W , Jeong MH , Cho JG , Park JC , Kang JC .
The Heart Center of Chonnam National University Hospital, Gwangju, Korea. cecilyk@hanmail.net
Abstract

BACKGROUND AND OBJECTIVES: Curcumin, a yellow pigment of turmeric in curry, has been reported to interfere with nuclear factor (NF)-kappaB. This study was designed to investigate the underlying pathway of the anti-inflammation effect of curcumin on endothelial cells. MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were stimulated with tumor necrosis factor (TNF)-alpha (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-kappaB) activation was determined by the NF-kappaB p65 translocation to the nucleus via immunocytochemistry. The expression of the NF-kappaB 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. RESULTS: Curcumin blocked the activation of NF-kappaB by TNF-alpha, and it also reduced the ROS, monocyte adhesion and the phosphorylation of JNK, p38 and STAT-3 in the TNF-alpha-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. CONCLUSION: We suggest that curcumin could contribute to protection against the adverse vascular effects of the pro-inflammatory response through the modulation of NF-kappaB, JNK, p38 and STAT-3, and this is in addition to its antioxidant effect in endothelial cells.

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