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Updated: Aug 7, 2026

On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Effects of cinnamic acid on expression of tissue factor induced by TNFalpha in endothelial cells and its mechanisms
Xiaofei Li1, Zhibin Wen, Xiaofan He
1Hemostasis Physiology Laboratory, Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, PR China.
Background:
To 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.
Methods:
Cellular 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.
Results:
CINN (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.
Conclusion:
CINN is able to attenuate TNFa-induced TF expression of vascular endothelial cells by inhibiting NF-kappaB activation.
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