Curcumin attenuates inflammatory responses of TNF-α-stimulated human endothelial cells
Curcumin attenuates inflammatory responses of TNF-α-stimulated human endothelial cells
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DOI：
10.1097/fjc.0b013e31805559b9
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发表时间：
2007-07-01
影响因子：
3
通讯作者：
Kang, Jung Chaee
中科院分区：
文献类型：
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作者：
Kim, Yong Sook;Ahn, Youngkeun;Kang, Jung Chaee
姜黄素是咖喱中姜黄的一种黄色色素，据报道会干扰核因子（NF）-κ B。本研究旨在探讨姜黄素对内皮细胞的抗炎作用机制。用10 ng/mL肿瘤坏死因子（TNF）-α刺激人脐静脉内皮细胞（HUVEC）。姜黄素阻断TNF-α对NF-κ B B的激活。姜黄素还减少了TNF-α刺激的HUVEC中的细胞内活性氧（ROS）、单核细胞粘附、c-Jun N-末端激酶（JNK）、p38和信号转导和转录激活因子（STAT）-3的磷酸化。姜黄素可在mRNA和蛋白水平上抑制细胞间粘附分子（ICAM）-1、单核细胞趋化蛋白（MCP）-1和白细胞介素（IL）-8的表达。然而，姜黄素并不影响TNF-α刺激的HUVECs中TNF受体I和11的表达。我们认为，姜黄素可以通过调节内皮细胞中的p38和STAT-3以及NF-κ B和JNK来保护血管免受促炎反应的不良影响。
Curcumin, a yellow pigment of turmeric in curry, is reported to interfere with nuclear factor (NF)-kappa B. 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-kappa B 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 11 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-kappa B and JNK in endothelial cells.