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Indole‐3‐carbinol suppressed inflammation‐associated factors in mice fed with high‐fat diet and in cocultured cells
Author(s) -
CHANG HSIAOPEI,
CHEN YUEHWA
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.541.3
Subject(s) - inflammation , endocrinology , medicine , adipose tissue , adipose tissue macrophages , nitric oxide synthase , adipocyte , nitric oxide , tumor necrosis factor alpha , monocyte , chemistry , macrophage , infiltration (hvac) , biology , white adipose tissue , biochemistry , physics , in vitro , thermodynamics
This study was aimed at investigating the effects of indole‐3‐carbinol (I3C), a cruciferous vegetable derivative, on obesity‐associated macrophage infiltration and inflammatory changes in animals and in cocultured cells. Male C57BL/6 mice were fed with high fat (HF) diet and HF diet + i.p. I3C (HFI) for 12 wk, and epididymal adipose tissue was collected for detection of the macrophage marker, F4/80. The results showed that I3C suppressed the HF diet‐induced macrophage infiltration in adipose tissue. To obtain the further insight of I3C on obesity‐associated inflammation, murine primary adipocytes were co‐cultured with RAW 264.7 macrophages, and the effects of I3C on inflammatory mediators, including nitric oxide (NO), interleukin‐6 (IL‐6), and monocyte chemoattractant protein‐1 (MCP‐1), were analyzed. The results indicated that I3C attenuated the productions of NO, MCP‐1, and IL‐6 in co‐cultured medium, suppressed inducible nitric oxide synthase (iNOS) mRNA expression, but enhanced peroxisome proliferators‐activator receptor (PPAR‐γ) mRNA expression. In conclusion, I3C reduced macrophage infiltration in HF diet‐fed animals, as well as suppressed pro‐inflammatory cytokines and modulated mRNA expression of iNOS and PPAR‐γ in adipocyte/macrophage co‐cultured cells.