Abstract
Piceatannol (PIC), a natural analog of resveratrol (RES), is a phytochemical found in passion fruit seeds. To clarify the effects of PIC on obesity‐induced inflammation in adipose tissue, we investigated the anti‐inflammatory activity of PIC‐related compounds (PIC, RES, and metabolites from PIC) in culture models of obese adipose tissue. Lipopolysaccharide (LPS) and conditioned medium from 3T3‐L1 adipocytes (3T3‐L1‐CM) enhanced proinflammatory gene expression and synthesis of nitric oxide (NO), tumor necrosis factor‐α (TNF‐α), and interleukin‐6 (IL‐6) in RAW264.7 macrophages. Although each compound inhibited the mRNA expression of iNOS (inducible NO synthase), TNF‐α, and IL‐6, PIC potently inhibited them, and 30 μmol/L PIC suppressed the LPS‐ and 3T3‐L1‐CM‐induced mRNA expression of iNOS (70.4% and 69.2% suppression, respectively), TNF‐α (42.6% and 47.0% suppression), and IL‐6 (27.3% and 42.1% suppression). PIC also significantly suppressed production of NO (80.3% suppression) and inflammatory cytokines (TNF‐α; 33.7% suppression, IL‐6; 66.5% suppression). Furthermore, PIC was found to rescue the uncoupling protein 1 mRNA expression induced by isoproterenol in 10T1/2 adipocytes, which was suppressed by LPS‐activated macrophages. These results suggest that PIC may attenuate the pathologic inflammation triggered by adipose tissues.
Highlights
Obesity is characterized by excessive accumulation of white adipose tissue (WAT)
This interaction is believed to occur via the release of monocyte chemoattractant protein-1 by hypertrophied adipocytes, which leads to the infiltration of macrophages into adipose tissue (Kanda et al 2006)
We investigated its effects on the inflammatory changes that result from the interaction of activated macrophages with two types of adipocytes
Summary
Obesity is characterized by excessive accumulation of white adipose tissue (WAT). This tissue is composed of various cell types, including mature adipocytes, preadipocytes, fibroblasts, endothelial cells, and macrophages. Recent studies have revealed that low-g rade chronic inflammation caused by macrophages interacting with hypertrophied adipocytes can lead to metabolic syndrome (i.e., cardiovascular disease, insulin resistance, type 2 diabetes, and hypertension) (Fernández-R eal and Ricart 2003; Dandona et al 2004). This interaction is believed to occur via the release of monocyte chemoattractant protein-1 by hypertrophied adipocytes, which leads to the infiltration of macrophages into adipose tissue (Kanda et al 2006). Inhibition of the chronic inflammation within WAT is an important therapeutic strategy in the treatment of insulin resistance
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