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      Phyllostachys edulis Compounds Inhibit Palmitic Acid-Induced Monocyte Chemoattractant Protein 1 (MCP-1) Production

      1 , 2 , 2 , 1 , *

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          Phyllostachys edulis Carriere (Poaceae) is a bamboo species that is part of the traditional Chinese medicine pharmacopoeia. Compounds and extracts from this species have shown potential applications towards several diseases. One of many complications found in obesity and diabetes is the link between elevated circulatory free fatty acids (FFAs) and chronic inflammation. This study aims to present a possible application of P. edulis extract in relieving inflammation caused by FFAs. Monocyte chemoattractant protein 1 (MCP-1/CCL2) is a pro-inflammatory cytokine implicated in chronic inflammation. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein 1 (AP-1) are transcription factors activated in response to inflammatory stimuli, and upregulate pro-inflammatory cytokines such as MCP-1. This study examines the effect of P. edulis extract on cellular production of MCP-1 and on the NF-κB and AP-1 pathways in response to treatment with palmitic acid (PA), a FFA.

          Methodology/Principal Findings

          MCP-1 protein was measured by cytometric bead assay. NF-κB and AP-1 nuclear localization was detected by colorimetric DNA-binding ELISA. Relative MCP-1 mRNA was measured by real-time quantitative PCR. Murine cells were treated with PA to induce inflammation. PA increased expression of MCP-1 mRNA and protein, and increased nuclear localization of NF-κB and AP-1. Adding bamboo extract (BEX) inhibited the effects of PA, reduced MCP-1 production, and inhibited nuclear translocation of NF-κB and AP-1 subunits. Compounds isolated from BEX inhibited MCP-1 secretion with different potencies.


          PA induced MCP-1 production in murine adipose, muscle, and liver cells. BEX ameliorated PA-induced production of MCP-1 by inhibiting nuclear translocation of NF-κB and AP-1. Two O-methylated flavones were isolated from BEX with functional effects on MCP-1 production. These results may represent a possible therapeutic application of BEX and its compounds toward alleviating chronic inflammation caused by elevated circulatory FFAs.

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          Most cited references 53

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          Obesity is associated with macrophage accumulation in adipose tissue.

          Obesity alters adipose tissue metabolic and endocrine function and leads to an increased release of fatty acids, hormones, and proinflammatory molecules that contribute to obesity associated complications. To further characterize the changes that occur in adipose tissue with increasing adiposity, we profiled transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob). We found that the expression of 1,304 transcripts correlated significantly with body mass. Of the 100 most significantly correlated genes, 30% encoded proteins that are characteristic of macrophages and are positively correlated with body mass. Immunohistochemical analysis of perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue revealed that the percentage of cells expressing the macrophage marker F4/80 (F4/80+) was significantly and positively correlated with both adipocyte size and body mass. Similar relationships were found in human subcutaneous adipose tissue stained for the macrophage antigen CD68. Bone marrow transplant studies and quantitation of macrophage number in adipose tissue from macrophage-deficient (Csf1op/op) mice suggest that these F4/80+ cells are CSF-1 dependent, bone marrow-derived adipose tissue macrophages. Expression analysis of macrophage and nonmacrophage cell populations isolated from adipose tissue demonstrates that adipose tissue macrophages are responsible for almost all adipose tissue TNF-alpha expression and significant amounts of iNOS and IL-6 expression. Adipose tissue macrophage numbers increase in obesity and participate in inflammatory pathways that are activated in adipose tissues of obese individuals.
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            NF-kappaB: a key role in inflammatory diseases.

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              Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases.


                Author and article information

                Role: Editor
                PLoS One
                PLoS ONE
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                18 September 2012
                27 September 2012
                : 7
                : 9
                [1 ]Department of Cell and Molecular Biology, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii, United States of America
                [2 ]Department of Chemistry, University of Hawaii at Manoa, Honolulu, Hawaii, United States of America
                University of Leuven, Rega Institute, Belgium
                Author notes

                Competing Interests: The authors maintain that there is no conflict of interest with regards to the cited patent (Chinese invention patent, CN1287848A). The patent belongs to Golden Basin Bio-Tech, and we have no ownership of their patent. The bamboo extract used in this study was donated to us by Golden Basin. We have no ownership or financial investment in Golden Basin, nor are receiving any remuneration or compensation from Golden Basin for our studies. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.

                Conceived and designed the experiments: JKH JP. Performed the experiments: JKH ZL. Analyzed the data: JKH ZL. Contributed reagents/materials/analysis tools: PW JP. Wrote the paper: JKH JP.


                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Pages: 11
                This work was supported by grants R21 AT003874 (Panee) and R21 AT005139 (Panee) from the National Center for Complementary and Alternative Medicine (NCCAM); grant U54RR022762 (RTRN Small Grant Program) from the National Center for Research Resources; grants from the National Center for Research Resources (5 G12 RR003061) and the National Institute on Minority Health and Health Disparities (8 G12 MD007601) from the National Institutes of Health; grants from the National Center for Research Resources (5P20RR016467-11) and the National Institute of General Medical Sciences (8 P20 GMl 03466-11) from the National Institutes of Health; and grant 5P20 MD000173-08 from National Center on Minority Health and Health Disparities (NCMHD). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Research Article
                Fatty Acids
                Drug Discovery
                Immune System
                Molecular Cell Biology
                Signal Transduction
                Signaling in Cellular Processes
                Clinical Immunology
                Immune System
                Complementary and Alternative Medicine
                Drugs and Devices
                Drug Research and Development
                Drug Discovery



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