Capsaicin attenuates palmitate-induced expression of macrophage inflammatory protein 1 and interleukin 8 by increasing palmitate oxidation and reducing c-Jun activation in THP-1 (human acute monocytic leukemia cell) cells |
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Authors: | Sung-E Choi Tae Ho Kim Sang-A YiYun Cheong Hwang Won Sun HwangSun Jung Choe Seung Jin HanHae Jin Kim Dae Jung KimYup Kang Kwan-Woo Lee |
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Affiliation: | a Department of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 443-749, Republic of Koreab BK21 Division of Cell Transformation and Restoration, Ajou University School of Medicine, Suwon 443-749, Republic of Koreac Division of Endocrinology, Department of Internal Medicine, Kwandong University, College of Medicine, Myongji Hospital, Goyang 697-24, Republic of Koread Department of Clinical Nutrition, Ajou University School of Medicine, Suwon 443-749, Republic of Koreae Institute of Medical Science, Ajou University School of Medicine, Suwon 443-749, Republic of Korea |
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Abstract: | Capsaicin, a spicy component of hot peppers, has been shown to improve inflammatory disease and obesity. In this study, we tested the hypothesis that the anti-inflammatory activity of capsaicin can be used to improve free fatty acid (FFA)-induced inflammation by reducing gene expression of macrophage inflammatory protein 1 (MIP-1) and interleukin 8 (IL-8) in THP-1 (human acute monocytic leukemia cell) macrophages. To investigate whether capsaicin ameliorates palmitate-induced MIP-1 and IL-8 gene expressions, we treated THP-1 cells with palmitate in the presence or absence of capsaicin and measured MIP-1 and IL-8 by real-time polymerase chain reaction. To elucidate the mechanism by which capsaicin effects on palmitate-induced MIP-1 and IL-8 gene expressions, we performed immunoblotting with stress kinase-related antibodies and measured palmitate oxidation and palmitate oxidation-related gene expression. Palmitate and stearate but not the unsaturated FFA oleate significantly increased MIP-1 and IL-8 expressions in THP-1 macrophages. Treatment with capsaicin or FFA oxidation stimulators inhibited palmitate-induced MIP-1 and IL-8 expressions in THP-1 macrophages. Capsaicin increased the gene expression of carnitine palmitoyltransferase 1 and the β-oxidation of palmitate. Furthermore, capsaicin significantly reduced palmitate-stimulated activation of c-Jun N-terminal kinase, c-Jun, and p38. Our data suggest that the attenuation of palmitate-induced MIP-1 and IL-8 gene expressions by capsaicin is associated with reduced activation of c-Jun N-terminal kinase, c-Jun, and p38 and preserved β-oxidation activity. |
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Keywords: | AICAR, aminoimidazole carboxamide ribonucleotide AMPK, AMP-activated protein kinase BSA, bovine serum albumin CoA, coenzyme A CPT-1, carnitine palmitoyltransferase 1 DAG, diacylglycerol eIF2α, eukaryotic translation initiation factor 2α ER, endoplasmic reticulum FFA, free fatty acid GAPDH, glyceraldehyde 3-phosphate dehydrogenase IL-6, interleukin 6 IL-8, interleukin 8 JNK, c-Jun N-terminal kinase LPS, lipopolysaccharide MCAD, medium-chain acyl-CoA dehydrogenase MCP-1, monocyte chemoattractant protein 1 MIP-1, macrophage inflammatory protein 1 mRNA, messenger RNA NF-κB, nuclear factor κB PCR, polymerase chain reaction PKC, protein kinase C PPAR-α, peroxisome proliferator-activated receptor α PPAR-γ, peroxisome proliferator-activated receptor γ ROS, reactive oxygen species RT-PCR, real-time polymerase chain reaction SDS, sodium dodecyl sulfate TLR-4, Toll-like receptor 4 TNF-α, tumor necrosis factor α VLCAD, very long chain acyl-CoA dehydrogenase |
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