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Lycopene inhibits TNF-alpha-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion.
Eur J Pharmacol. 2008 May 31; 586(1-3):275-82.EJ

Abstract

Inflammatory mediators such as TNF-alpha and interleukin (IL)-1beta, and IL-8, which can enhance binding of low-density lipoprotein (LDL) to endothelium and upregulate expression of leukocyte adhesion molecules on endothelium during atherogenesis. Lycopene, a natural carotenoid from tomato and other sources, has been shown to prevent cardiovascular diseases in epidemiological studies. However, its anti-inflammatory action mechanism remains unclear. In the present study, we studied the effect of lycopene on TNF-alpha-induced signaling in human umbilical endothelial cells (HUVECs). We found that TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression in HUVECs was inhibited by lycopene, whereas cyclooxygenase-2 (COX-2) and platelet-endothelial cell adhesion molecule (PECAM-1) expression were not affected. A further analysis indicated that lycopene attenuated TNF-alpha-induced IkappaB phosphorylation, NF-kappaB expression, and NF-kappaB p65 translocation from cytosol to nucleus. In line with this, TNF-alpha-induced NF-kappaB-DNA but not AP1-DNA complexes formation was inhibited by lycopene, as determined by the electrophoretic mobility shift assay (EMSA). On the other hand, lycopene did not affect TNF-alpha-induced p38 and extracellular matrix-regulated kinase1/2 (ERK1/2) phosphorylation and interferon-gamma (IFN-gamma)-induced signaling, suggesting that lycopene primarily affects TNF-alpha-induced NF-kappaB signaling pathway. In a functional study, lycopene dose-dependently attenuated monocyte adhesion to endothelial monolayer but not that adhesion to extracellular matrix. Taken together, we provided here the first evidence showing that lycopene is able to inhibit TNF-alpha-induced NF-kappaB activation, ICAM-1 expression, and monocyte-endothelial interaction, suggesting an anti-inflammatory role of lycopene and possibly explaining in part why lycopene can prevent cardiovascular diseases.

Authors+Show Affiliations

School of Medicine, Fu-Jen Catholic University, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18439578

Citation

Hung, Chi-Feng, et al. "Lycopene Inhibits TNF-alpha-induced Endothelial ICAM-1 Expression and Monocyte-endothelial Adhesion." European Journal of Pharmacology, vol. 586, no. 1-3, 2008, pp. 275-82.
Hung CF, Huang TF, Chen BH, et al. Lycopene inhibits TNF-alpha-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion. Eur J Pharmacol. 2008;586(1-3):275-82.
Hung, C. F., Huang, T. F., Chen, B. H., Shieh, J. M., Wu, P. H., & Wu, W. B. (2008). Lycopene inhibits TNF-alpha-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion. European Journal of Pharmacology, 586(1-3), 275-82. https://doi.org/10.1016/j.ejphar.2008.03.001
Hung CF, et al. Lycopene Inhibits TNF-alpha-induced Endothelial ICAM-1 Expression and Monocyte-endothelial Adhesion. Eur J Pharmacol. 2008 May 31;586(1-3):275-82. PubMed PMID: 18439578.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lycopene inhibits TNF-alpha-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion. AU - Hung,Chi-Feng, AU - Huang,Tur-Fu, AU - Chen,Bing-Huei, AU - Shieh,Jiunn-Min, AU - Wu,Pi-Hui, AU - Wu,Wen-Bin, Y1 - 2008/03/13/ PY - 2007/11/19/received PY - 2008/02/22/revised PY - 2008/03/03/accepted PY - 2008/4/29/pubmed PY - 2008/9/3/medline PY - 2008/4/29/entrez SP - 275 EP - 82 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 586 IS - 1-3 N2 - Inflammatory mediators such as TNF-alpha and interleukin (IL)-1beta, and IL-8, which can enhance binding of low-density lipoprotein (LDL) to endothelium and upregulate expression of leukocyte adhesion molecules on endothelium during atherogenesis. Lycopene, a natural carotenoid from tomato and other sources, has been shown to prevent cardiovascular diseases in epidemiological studies. However, its anti-inflammatory action mechanism remains unclear. In the present study, we studied the effect of lycopene on TNF-alpha-induced signaling in human umbilical endothelial cells (HUVECs). We found that TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression in HUVECs was inhibited by lycopene, whereas cyclooxygenase-2 (COX-2) and platelet-endothelial cell adhesion molecule (PECAM-1) expression were not affected. A further analysis indicated that lycopene attenuated TNF-alpha-induced IkappaB phosphorylation, NF-kappaB expression, and NF-kappaB p65 translocation from cytosol to nucleus. In line with this, TNF-alpha-induced NF-kappaB-DNA but not AP1-DNA complexes formation was inhibited by lycopene, as determined by the electrophoretic mobility shift assay (EMSA). On the other hand, lycopene did not affect TNF-alpha-induced p38 and extracellular matrix-regulated kinase1/2 (ERK1/2) phosphorylation and interferon-gamma (IFN-gamma)-induced signaling, suggesting that lycopene primarily affects TNF-alpha-induced NF-kappaB signaling pathway. In a functional study, lycopene dose-dependently attenuated monocyte adhesion to endothelial monolayer but not that adhesion to extracellular matrix. Taken together, we provided here the first evidence showing that lycopene is able to inhibit TNF-alpha-induced NF-kappaB activation, ICAM-1 expression, and monocyte-endothelial interaction, suggesting an anti-inflammatory role of lycopene and possibly explaining in part why lycopene can prevent cardiovascular diseases. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/18439578/Lycopene_inhibits_TNF_alpha_induced_endothelial_ICAM_1_expression_and_monocyte_endothelial_adhesion_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(08)00269-0 DB - PRIME DP - Unbound Medicine ER -