Xanthones from Mangosteen Inhibit Inflammation in Human Macrophages and in Human Adipocytes Exposed to Macrophage-Conditioned Media  

Oleh:

Bumrungpert, Akkarach ; Kalpravidh, Ruchaneekorn W. ; Chia-Chi, Chuang ; Overman, Angel ; Martinez, Kristina

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 140 no. 04 (Apr. 2010), page 842.

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2010.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Obesity-associated inflammation is characterized by recruitment of macrophages (M{Phi}) into white adipose tissue (WAT) and production of inflammatory cytokines, leading to the development of insulin resistance. The xanthones, {alpha}- and {gamma}-mangostin (MG), are major bioactive compounds found in mangosteen that are reported to have antiinflammatory and antioxidant properties. Thus, we examined the efficacy of MG to prevent lipopolysaccharide (LPS)-mediated inflammation in human M{Phi} (differentiated U937 cells) and cross-talk with primary cultures of newly differentiated human adipocytes. We found that {alpha}- and {gamma}-MG attenuated LPS-induced expression of inflammatory genes, including tumor necrosis factor-{alpha}, interleukin-6, and interferon {gamma}-inducible protein-10 in a dose-dependent manner in M{Phi}. We also found that {alpha}- and {gamma}-MG attenuated LPS-activated mitogen-activated protein kinases (MAPK) and activator protein (AP)-1, but only {gamma}-MG reduced nuclear factor-{kappa}B (NF-{kappa}B). In addition, {alpha}- and {gamma}-MG attenuated LPS suppression of PPAR{gamma} gene expression in a dose-dependent manner. Notably, the ability of M{Phi}-conditioned media to cause inflammation and insulin resistance in primary cultures of human adipocytes was attenuated by pretreating M{Phi} with {gamma}-MG. Taken together, these data demonstrate that MG attenuates LPS-mediated inflammation in M{Phi} and insulin resistance in adipocytes, possibly by preventing the activation of MAPK, NF-{kappa}B, and AP-1, which are central to inflammatory cytokine production in WAT.

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