Phyllostachys edulis compounds inhibit palmitic acid-induced monocyte chemoattractant protein 1 (MCP-1) production.

Phyllostachys edulis compounds inhibit palmitic acid-induced monocyte chemoattractant protein 1 (MCP-1) production.
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DOI:
10.1371/journal.pone.0045082
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Panee J
Panee J
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Higa JK;Liang Z;Williams PG;Panee J

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毛竹(Phyllostachys edulis卡里埃)是禾本科(Poaceae)竹类植物,是我国传统的药用植物。该物种的化合物和提取物已显示出对几种疾病的潜在应用。肥胖和糖尿病中发现的许多并发症之一是循环游离脂肪酸(FFA)升高与慢性炎症之间的联系。本研究的目的是提出一种可能的应用,紫丁香提取物在减轻由脂肪酸引起的炎症。单核细胞趋化蛋白1(MCP-1/CCL 2)是一种与慢性炎症有关的促炎细胞因子。活化B细胞的核因子κ-轻链增强子(NF-κB)和活化蛋白1(AP-1)是响应炎症刺激而活化的转录因子,并且上调促炎细胞因子如MCP-1。本研究检测了棕榄提取物对细胞产生MCP-1以及响应于棕榈酸(PA)(FFA)处理的NF-κB和AP-1途径的影响。MCP-1蛋白用流式细胞仪检测。DNA结合ELISA法检测NF-κB和AP-1的核定位。实时定量PCR检测MCP-1 mRNA的相对表达量。用PA处理鼠细胞以诱导炎症。PA可增加MCP-1 mRNA和蛋白的表达,增加NF-κB和AP-1的核定位。加入竹子提取物(BEX)可抑制PA的作用,减少MCP-1的产生,并抑制NF-κB和AP-1亚基的核转位。从BEX分离的化合物以不同的效力抑制MCP-1分泌。PA诱导小鼠脂肪、肌肉和肝细胞产生MCP-1。BEX通过抑制NF-κB和AP-1的核转位来改善PA诱导的MCP-1的产生。从BEX中分离出两种O-甲基化黄酮,对MCP-1的产生具有功能作用。这些结果可能代表了BEX及其化合物在缓解由循环FFA升高引起的慢性炎症方面的可能治疗应用。
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. 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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