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Anti‐Inflammatory Effects of Grape Powder Extract (GPE) in Human Macrophages
Author(s) -
Overman Angel,
Bumrungpert Akkarach,
Kennedy Arion,
Martinez Kristina,
West Tiffany,
Hopkins Robin,
Chuang ChiaChi,
McIntosh Michael
Publication year - 2009
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.23.1_supplement.717.14
Subject(s) - chemokine , p38 mitogen activated protein kinases , mapk/erk pathway , lipopolysaccharide , inflammation , nf κb , kinase , chemistry , macrophage inflammatory protein , protein kinase a , phosphorylation , activator (genetics) , iκbα , nfkb1 , tumor necrosis factor alpha , microbiology and biotechnology , biology , biochemistry , immunology , transcription factor , gene
Obesity‐associated inflammation is characterized by an increased abundance of macrophages in white adipose tissue (WAT), along with production of inflammatory cytokines, chemokines, and prostaglandins. Grape powder extract (GPE) is rich in phenolic phytochemicals that possess anti‐inflammatory properties. Thus, we examined the ability of GPE to prevent lipopolysaccharide (LPS)‐mediated activation of mitogen activated protein kinases (MAPK), nuclear factor kappa B (NF‐κB), and activator protein‐1 (AP‐1), and induction of inflammatory genes in human macrophages. Cultures of differentiated U937 cells were treated with LPS in the absence or presence of GPE. Pretreatment with GPE attenuated LPS‐induced expression of inflammatory cytokines (e.g., TNFα, IL‐6, IL‐1B,), chemokines (i.e., IL‐8, IP‐10), and a marker of prostaglandin production (COX‐2). GPE also attenuated LPS activation of MAPK, NFκB, and AP‐1 as evidenced by decreased 1) phosphorylation of c‐Jun NH2‐terminal kinase (JNK) and p38, 2) degradation of I?Bα, and 3) phosphorylation of c‐Jun. These data suggest that GPE attenuates LPS‐mediated inflammatory gene expression in human macrophages by decreasing the activation of MAPK, NFκB, and AP‐1. (Supported by the W.B. Kellogg Institute for Food and Nutrition Research) Grant Funding Source W.B Kellogg Institute for Food and Nutrition Research