• Xiaofei Li, Zhibin Wen, Xiaofan He, and Shilin He.
• Hemostasis Physiology Laboratory, Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, PR China.
• J Chin Med Assoc. 2006 May 1; 69 (5): 207-12.

BackgroundTo observe the effects of cinnamic acid (CINN) on the expression of tissue factor (TF) induced by tumor necrosis factor alpha (TNFalpha) in human umbilical vein endothelium-derived cell line (ECV304) and the related mechanisms.MethodsCellular TF activity was determined with 1-stage clotting assay in the presence or absence of anti-TF antibody or DEGR-Vlla. TF mRNA was examined by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). I-kappaB was measured by Western blot analysis. Immunohistochemical analysis was performed to evaluate the activation of NF-kappaB.ResultsCINN (500 microg/mL) significantly decreased the TF activity in ECV304 induced by TNFalpha (1000 U/mL) (p < 0.01) in a concentration-dependent fashion (r = -0.953, p < 0.05). CINN also inhibited the expression of TF mRNA induced by TNFalpha. Immunohistochemical analysis demonstrated NF-kappaB translocation from the cytoplasm to the nucleus, and Western blot analysis showed I-KB decrement in cytoplasm after treatment of endothelial cells with TNFalpha. CINN diminished these changes induced by TNFalpha.ConclusionCINN is able to attenuate TNFa-induced TF expression of vascular endothelial cells by inhibiting NF-kappaB activation.

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