| Literature DB >> 17666914 |
Yong Sook Kim1, Youngkeun Ahn, Moon Hwa Hong, Soo Yeon Joo, Kye Hun Kim, Il Suk Sohn, Hyung Wook Park, Young Joon Hong, Ju Han Kim, Weon Kim, Myung Ho Jeong, Jeong Gwan Cho, Jong Chun Park, Jung Chaee Kang.
Abstract
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.Entities:
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Year: 2007 PMID: 17666914 DOI: 10.1097/FJC.0b013e31805559b9
Source DB: PubMed Journal: J Cardiovasc Pharmacol ISSN: 0160-2446 Impact factor: 3.105