Quercetin attenuates inflammation in human macrophages and adipocytes exposed to macrophage-conditioned media
Quercetin attenuates inflammation in human macrophages and adipocytes exposed to macrophage-conditioned media
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DOI：
10.1038/ijo.2010.272
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发表时间：
2011-09-01
影响因子：
4.9
通讯作者：
McIntosh, M.
中科院分区：
文献类型：
--
作者：
Overman, A.;Chuang, C-C;McIntosh, M.
背景：肥胖与白色脂肪组织中的慢性炎症有关，而炎症会因巨噬细胞(MFS)的渗入而加重。我们最近证实，葡萄粉提取物(GPE)富含槲皮素(Que)，可以减轻人MFS的炎症，防止MF介导的炎症和人类脂肪细胞的胰岛素抵抗。然而，我们不知道Que是如何单独影响这些结果的。目的和设计：我们检测了Que对人MFS(即分化的U937细胞株)的炎症抑制程度以及与人脂肪细胞(即新分化的人类脂肪细胞的原代培养)的相互作用。方法和结果：Que处理MFS后，炎症基因的基础表达减少，如肿瘤坏死因子-a、白细胞介素6、IL-8、IL-1β和干扰素-g诱导蛋白-10，以及前列腺素产生的标志物环氧合酶-2。Que还可降低MFS中磷酸化c-Jun氨基末端激酶(JNK)和c-Jun的丰度及I-kappa Bα的降解。此外，经Que处理的MFS获得的条件培养液(CM)降低了该CM刺激脂肪细胞炎症和引起胰岛素抵抗的能力，这表现为：(1)炎症基因表达，(2)JNK和c-Jun的磷酸化，(3)胰岛素受体底物(IRS)-1的丝氨酸残基307的磷酸化，4)蛋白酪氨酸磷酸酶-1B基因的表达，5)抑制胰岛素刺激的血糖升高。结论：这些数据表明，Que是GPE的生物活性成分之一，可以预防MFS的炎症和MF介导的脂肪细胞的胰岛素抵抗。《国际肥胖杂志》(2011年)3511651172；doi：10.1038/ijo.2010.272；2011年1月11日在线发表
Background: Obesity is linked to chronic inflammation in white adipose tissue, which is exacerbated by infiltrating macrophages (MFs). We recently demonstrated that an extract from grape powder (GPE), which is abundant in quercetin (QUE), reduced inflammation in human MFs and prevented MF-mediated inflammation and insulin resistance in human adipocytes. However, we did not know how QUE individually affected these outcomes.Objective and design: We examined the extent to which QUE prevents inflammation in human MFs (that is, differentiated U937 cell line) and cross-talk with human adipocytes (that is, primary cultures of newly differentiated human adipocytes).Methods and results: Treatment of MFs with QUE attenuated the basal expression of inflammatory genes, such as tumor necrosis factor-a, interleukin (IL)-6, IL-8, IL-1 beta and interferon-g inducible protein-10, and cyclooxygenase-2, a marker of prostaglandin production. QUE also attenuated the abundance of phosphorylated c-Jun N-terminal kinase (JNK) and c-Jun, and I kappa B alpha degradation in MFs. Furthermore, conditioned media (CM) obtained from MFs treated with QUE decreased the capacity of this CM to inflame adipocytes and cause insulin resistance as evidenced by decreased: (1) inflammatory gene expression, (2) phosphorylation of JNK and c-Jun, (3) serine residue 307 phosphorylation of insulin receptor substrate (IRS)-1, 4) protein tyrosine phosphatase-1B gene expression and 5) suppression of insulin-stimulated glucose uptake.Conclusion: Taken together, these data suggest that QUE is one of the bioactive components of GPE that prevents inflammation in MFs and MF-mediated insulin resistance in adipocytes. International Journal of Obesity (2011) 35, 1165-1172; doi:10.1038/ijo.2010.272; published online 11 January 2011