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胡椒碱抑制 LPS 诱导的 RAW 264.7 细胞炎症介质的表达。

Piperine inhibits LPS induced expression of inflammatory mediators in RAW 264.7 cells.

机构信息

Department of Orthopaedic Surgery, The Second Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, China.

出版信息

Cell Immunol. 2013 Sep-Oct;285(1-2):49-54. doi: 10.1016/j.cellimm.2013.09.001. Epub 2013 Sep 11.

DOI:10.1016/j.cellimm.2013.09.001
PMID:24071564
Abstract

The aim of the present study was to investigate the effects of piperine on the inflammatory responses to lipopolysaccharide (LPS) in RAW264.7 cells and the signal transduction pathways involved. RAW264.7 cells were pretreated with piperine at 10, 50 or 100 μg/ml and subsequently stimulated with LPS (1 μg/ml) for 24 h. We found that piperine inhibited the production of prostaglandin E2 (PGE2) and nitric oxide (NO) induced by LPS. Piperine significantly decreased LPS-stimulated gene expression and production of tumor necrosis factor-alpha (TNF), inducible NO synthase (iNOS) and COX-2 in RAW264.7 cells. Piperine inhibited the LPS-mediated activation of nuclear factor-kappa B (NF-kappaB) by suppressing the degradation of inhibitor-κB proteins (IκB) and the translocations of p65 subunit of NF-kB from the cytosol to the nucleus. Our results demonstrate the anti-inflammatory activity of piperine in RAW264.7 cells; suggesting that piperine may be a potential agent in the treatment of inflammation.

摘要

本研究旨在探讨胡椒碱对脂多糖（LPS）诱导的 RAW264.7 细胞炎症反应的影响及其相关信号转导通路。RAW264.7 细胞用 10、50 或 100μg/ml 的胡椒碱预处理，然后用 1μg/ml 的 LPS 刺激 24 小时。结果发现，胡椒碱抑制了 LPS 诱导的前列腺素 E2（PGE2）和一氧化氮（NO）的产生。胡椒碱显著降低了 LPS 刺激的肿瘤坏死因子-α（TNF-α）、诱导型一氧化氮合酶（iNOS）和 COX-2 在 RAW264.7 细胞中的基因表达和产生。胡椒碱通过抑制抑制剂 κB 蛋白（IκB）的降解和 NF-κB p65 亚基从细胞质向核内的转位，抑制了 LPS 介导的核因子-κB（NF-κB）的激活。我们的研究结果表明胡椒碱在 RAW264.7 细胞中具有抗炎活性；提示胡椒碱可能是治疗炎症的潜在药物。

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