PMID- 28555020
OWN - NLM
STAT- MEDLINE
DCOM- 20180305
LR  - 20231112
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 18
IP  - 6
DP  - 2017 May 27
TI  - 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.
LID - 10.3390/ijms18061148 [doi]
LID - 1148
AB  - 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 muM, N-caffeoyltryptamine significantly inhibited p38 MAP 
      kinase alpha, beta, gamma and delta by 15-50% (p < 0.05), particularly p38 MAP kinase alpha (IC(50) 
      = 16.7 muM) and beta (IC(50) = 18.3 muM). Also, the pretreatment of the 
      lipopolysaccharide (LPS)-stimulated THP-1 cells with N-caffeoyltryptamine (10, 20 
      and 40 muM) 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.
FAU - Park, Jae B
AU  - Park JB
AD  - 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. 
      jae.park@ars.usda.gov.
LA  - eng
PT  - Journal Article
DEP - 20170527
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Amides)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Caffeic Acids)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (N-caffeoyltryptamine)
RN  - 0 (Tryptamines)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Amides/*pharmacology
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Caffeic Acids/*pharmacology
MH  - Chemokine CCL2/*metabolism
MH  - Diet, High-Fat/adverse effects
MH  - Humans
MH  - Lipopolysaccharides/*pharmacology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - THP-1 Cells
MH  - Tryptamines/*pharmacology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC5485972
OTO - NOTNLM
OT  - MCP-1
OT  - N-caffeoyltryptamine
OT  - high-fat diet
OT  - p38 MAP kinase
OT  - rats
COIS- The authors declare no conflict of interest.
EDAT- 2017/05/31 06:00
MHDA- 2018/03/06 06:00
PMCR- 2017/06/01
CRDT- 2017/05/31 06:00
PHST- 2017/02/03 00:00 [received]
PHST- 2017/05/22 00:00 [revised]
PHST- 2017/05/24 00:00 [accepted]
PHST- 2017/05/31 06:00 [entrez]
PHST- 2017/05/31 06:00 [pubmed]
PHST- 2018/03/06 06:00 [medline]
PHST- 2017/06/01 00:00 [pmc-release]
AID - ijms18061148 [pii]
AID - ijms-18-01148 [pii]
AID - 10.3390/ijms18061148 [doi]
PST - epublish
SO  - Int J Mol Sci. 2017 May 27;18(6):1148. doi: 10.3390/ijms18061148.