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番茄提取物可抑制脂肪细胞与巨噬细胞相互作用所诱导的促炎介质的产生。

Tomato extract suppresses the production of proinflammatory mediators induced by interaction between adipocytes and macrophages.

作者信息

Kim Young-il, Mohri Shinsuke, Hirai Shizuka, Lin Shan, Goto Tsuyoshi, Ohyane Chie, Sakamoto Tomoya, Takahashi Haruya, Shibata Daisuke, Takahashi Nobuyuki, Kawada Teruo

机构信息

a Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture , Kyoto University , Uji, Kyoto , Japan.

出版信息

Biosci Biotechnol Biochem. 2015;79(1):82-7. doi: 10.1080/09168451.2014.962472.

DOI:10.1080/09168451.2014.962472
PMID:25603813
Abstract

Obese adipose tissue is characterized by enhanced macrophage infiltration. A loop involving monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNFα) between adipocytes and macrophages establishes a vicious cycle that augments inflammatory changes and insulin resistance in obese adipose tissue. Tomatoes, one of the most popular crops worldwide, contain many beneficial phytochemicals that improve obesity-related diseases such as diabetes. Some of them have also been reported to have anti-inflammatory properties. In this study, we focused on the potential protective effects of phytochemicals in tomatoes on inflammation. We screened fractions of tomato extract using nitric oxide (NO) assay in lipopolysaccharide (LPS)-stimulated RAW264 macrophages. One fraction, RF52, significantly inhibited NO production in LPS-stimulated RAW264 macrophages. Furthermore, RF52 significantly decreased MCP-1 and TNFα productions. The coculture of 3T3-L1 adipocytes and RAW264 macrophages markedly enhanced MCP-1, TNFα, and NO productions compared with the control cultures; however, the treatment with RF52 inhibited the production of these proinflammatory mediators. These results suggest that RF52 from tomatoes may have the potential to suppress inflammation by inhibiting the production of NO or proinflammatory cytokines during the interaction between adipocytes and macrophages.

摘要

肥胖脂肪组织的特征是巨噬细胞浸润增强。脂肪细胞与巨噬细胞之间存在一个涉及单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子-α(TNFα)的循环,形成了一个恶性循环,加剧了肥胖脂肪组织中的炎症变化和胰岛素抵抗。番茄是全球最受欢迎的作物之一,含有许多有益的植物化学物质,可改善肥胖相关疾病,如糖尿病。其中一些还被报道具有抗炎特性。在本研究中,我们重点关注番茄中的植物化学物质对炎症的潜在保护作用。我们在脂多糖(LPS)刺激的RAW264巨噬细胞中使用一氧化氮(NO)测定法筛选番茄提取物的组分。其中一个组分RF52显著抑制LPS刺激的RAW264巨噬细胞中NO的产生。此外,RF52显著降低MCP-1和TNFα的产生。与对照培养相比,3T3-L1脂肪细胞与RAW264巨噬细胞的共培养显著增强了MCP-1、TNFα和NO的产生;然而,用RF52处理可抑制这些促炎介质的产生。这些结果表明,番茄中的RF52可能具有通过在脂肪细胞与巨噬细胞相互作用期间抑制NO或促炎细胞因子的产生来抑制炎症的潜力。

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