J Cardiovasc Pharmacol. 2007 Jul;50(1):41-9.

Curcumin attenuates inflammatory responses of TNF-alpha-stimulated human endothelial cells.

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.

Heart Center of Chonnam National University Hospital, Gwangju, South Korea.

Curcumin,
a yellow pigment of turmeric in curry, is reported to interfere with
nuclear factor (NF)-kappaB. This study was designed to investigate the
underlying pathway of antiinflammation of curcumin on endothelial
cells. Human umbilical vein endothelial cells (HUVECs) were stimulated
with 10 ng/mL tumor necrosis factor (TNF)-alpha. Curcumin blocked the
activation of NF-kappaB by TNF-alpha. Curcumin also reduced the
intracellular reactive oxygen species (ROS), monocyte adhesion,
phosphorylation of c-Jun N-terminal kinase (JNK), p38, and signal
transducer and activator of transcription (STAT)-3 in
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 mRNA and
protein level. Curcumin, however, did not affect the expression of TNF
receptor I and II in TNF-alpha-stimulated HUVECs. We suggest that
curcumin could contribute to protection against the adverse vascular
effect of the proinflammatory response through the modulation of p38
and STAT-3 in addition to NF-kappaB and JNK in endothelial cells.

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