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Int. J. Mol. Sci. 2017, 18(6), 1148; doi:10.3390/ijms18061148

N-Caffeoyltryptamine, a Potent Anti-Inflammatory Phenolic Amide, Suppressed MCP-1 Expression in LPS-stimulated THP-1 Cells and Rats Fed a High-Fat Diet

Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, The Agricultural Research Service, The United States Department of Agriculture, Bldg. 307C, Rm. 131, Beltsville, MD 20705, USA
Academic Editor: Manickam Sugumaran
Received: 3 February 2017 / Revised: 22 May 2017 / Accepted: 24 May 2017 / Published: 27 May 2017
(This article belongs to the Section Bioactives and Nutraceuticals)
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Abstract

Monocyte chemoattractant protein-1 (MCP-1) is a well-known chemokine critically involved in the pathophysiological progression of several inflammatory diseases including arthrosclerosis. N-caffeoyltryptamine is a phenolic amide with strong anti-inflammatory effects. Therefore, in this paper, the potential effect of N-caffeoyltryptamine on MCP-1 expression was investigated as a potential p38 mitogen-activated protein (MAP) kinase inhibitor in vitro and in vivo. At the concentration of 20 μM, N-caffeoyltryptamine significantly inhibited p38 MAP kinase α, β, γ and δ by 15–50% (p < 0.05), particularly p38 MAP kinase α (IC50 = 16.7 μM) and β (IC50 = 18.3 μM). Also, the pretreatment of the lipopolysaccharide (LPS)-stimulated THP-1 cells with N-caffeoyltryptamine (10, 20 and 40 μM) led to significant suppression of MCP-1 production by 10–45% (p < 0.05) in the cells. Additionally, N-caffeoyltryptamine was also able to significantly downregulate MCP-1 mRNA expression in the THP-1 cells (p < 0.05). On the basis of this strong inhibition in vitro, an animal study was conducted to confirm this inhibitory effect in vivo. Rats were divided into three groups (n = 8): a normal control diet (C), a high-fat diet (HF), or a high-fat diet supplemented with N-caffeoyltryptamine (2 mg per day) (HFS). After 16 weeks, blood samples were collected from the rats in each group, and MCP-1 levels were determined in plasma with other atherogenic markers (C-reactive protein and soluble E-selectin (sE-selectin)). As expected, the average MCP-1 levels of the HF group were found to be higher than those of the C group (p < 0.05). However, the MCP-1 levels of the HFS group were significantly lower than those of the HF group (p < 0.05), suggesting that N-caffeoyltryptamine could decrease MCP-1 expression in vivo. Related to other atherogenic markers such as C-reactive protein and sE-selectin, there was no significant difference in their levels between the HF and HFS groups. These data suggest that N-caffeoyltryptamine may specifically suppress MCP-1 expression in vitro and in vivo, possibly by inhibiting p38 MAP kinase. View Full-Text
Keywords: N-caffeoyltryptamine; p38 MAP kinase; MCP-1; high-fat diet; rats N-caffeoyltryptamine; p38 MAP kinase; MCP-1; high-fat diet; rats
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MDPI and ACS Style

Park, J.B. N-Caffeoyltryptamine, a Potent Anti-Inflammatory Phenolic Amide, Suppressed MCP-1 Expression in LPS-stimulated THP-1 Cells and Rats Fed a High-Fat Diet. Int. J. Mol. Sci. 2017, 18, 1148.

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