PMID- 17196622
OWN - NLM
STAT- MEDLINE
DCOM- 20070320
LR  - 20240109
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 80
IP  - 10
DP  - 2007 Feb 13
TI  - Active spice-derived components can inhibit inflammatory responses of adipose 
      tissue in obesity by suppressing inflammatory actions of macrophages and release 
      of monocyte chemoattractant protein-1 from adipocytes.
PG  - 926-31
AB  - Inflammation plays a key role in obesity-related pathologies such as 
      cardiovascular disease, type II diabetes, and several types of cancer. 
      Obesity-induced inflammation entails the enhancement of the recruitment of 
      macrophages into adipose tissue and the release of various proinflammatory 
      proteins from fat tissue. Therefore, the modulation of inflammatory responses in 
      obesity may be useful for preventing or ameliorating obesity-related pathologies. 
      Some spice-derived components, which are naturally occurring phytochemicals, 
      elicit antiobesity and antiinflammatory properties. In this study, we 
      investigated whether active spice-derived components can be applied to the 
      suppression of obesity-induced inflammatory responses. Mesenteric adipose tissue 
      was isolated from obese mice fed a high-fat diet and cultured to prepare an 
      adipose tissue-conditioned medium. Raw 264.7 macrophages were treated with the 
      adipose tissue-conditioned medium with or without active spice-derived components 
      (i.e., diallyl disulfide, allyl isothiocyanate, piperine, zingerone and 
      curcumin). Chemotaxis assay was performed to measure the degree of macrophage 
      migration. Macrophage activation was estimated by measuring tumor necrosis 
      factor-alpha (TNF-alpha), nitric oxide, and monocyte chemoattractant protein-1 
      (MCP-1) concentrations. The active spice-derived components markedly suppressed 
      the migration of macrophages induced by the mesenteric adipose tissue-conditioned 
      medium in a dose-dependent manner. Among the active spice-derived components 
      studied, allyl isothiocyanate, zingerone, and curcumin significantly inhibited 
      the cellular production of proinflammatory mediators such as TNF-alpha and nitric 
      oxide, and significantly inhibited the release of MCP-1 from 3T3-L1 adipocytes. 
      Our findings suggest that the spice-derived components can suppress 
      obesity-induced inflammatory responses by suppressing adipose tissue macrophage 
      accumulation or activation and inhibiting MCP-1 release from adipocytes. These 
      spice-derived components may have a potential to improve chronic inflammatory 
      conditions in obesity.
FAU - Woo, Hae-Mi
AU  - Woo HM
AD  - Department of Food Science and Nutrition, University of Ulsan, Mugeo-Dong, 
      Nam-Ku, Ulsan, South Korea.
FAU - Kang, Ji-Hye
AU  - Kang JH
FAU - Kawada, Teruo
AU  - Kawada T
FAU - Yoo, Hoon
AU  - Yoo H
FAU - Sung, Mi-Kyung
AU  - Sung MK
FAU - Yu, Rina
AU  - Yu R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20061123
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/drug effects/*metabolism/*pathology
MH  - Adipose Tissue/*pathology
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemotaxis/drug effects
MH  - Culture Media, Conditioned
MH  - Macrophages/*drug effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nitric Oxide/metabolism
MH  - Obesity/*pathology
MH  - Spices/*analysis
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2007/01/02 09:00
MHDA- 2007/03/21 09:00
CRDT- 2007/01/02 09:00
PHST- 2006/08/31 00:00 [received]
PHST- 2006/10/24 00:00 [revised]
PHST- 2006/11/13 00:00 [accepted]
PHST- 2007/01/02 09:00 [pubmed]
PHST- 2007/03/21 09:00 [medline]
PHST- 2007/01/02 09:00 [entrez]
AID - S0024-3205(06)00912-X [pii]
AID - 10.1016/j.lfs.2006.11.030 [doi]
PST - ppublish
SO  - Life Sci. 2007 Feb 13;80(10):926-31. doi: 10.1016/j.lfs.2006.11.030. Epub 2006 
      Nov 23.