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首页> 外文期刊>Inflammation >Salicylate Inhibits Macrophage-Secreted Factors Induced Adipocyte Inflammation and Changes of Adipokines in 3T3-L1 Adipocytes
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Salicylate Inhibits Macrophage-Secreted Factors Induced Adipocyte Inflammation and Changes of Adipokines in 3T3-L1 Adipocytes

机译:水杨酸盐抑制巨噬细胞分泌因子诱导的脂肪细胞炎症和3T3-L1脂肪细胞中脂肪因子的变化。

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摘要

Antidiabetic effects of salicylates have been known for years, however the cellular and molecular mechanisms of the hypoglycemic activity are not well elucidated. We examined the effects of salicylate on inflammation-related changes in gene or/and protein expressions of several adipokines in 3T3-L1 adipocytes and of LPS-induced inflammatory factors in RAW 264.7 cell. Especially, we focused our attention on the cross-talk between the macrophages and adipocytes. Exposure to RAW-CM medium resulted in an increase in the gene expression or/and protein secretion of TNF-α, IL-6 and resistin, and at the same time, a decrease in the gene expression of PPARγ and adiponectin in 3T3-L1 adipocytes. Salicylate effectively reversed these changes, and up-regulated glucose consumption in adipocytes. We also found salicylate inhibited phosphorylation of NF-κB in RAW-CM-stimulated adipocytes. We conclude salicylate blocks inflammatory process in the pathogenesis of inflammation-related insulin resistance.
机译:水杨酸酯的抗糖尿病作用已为人所知,但是降血糖活性的细胞和分子机制尚未得到很好的阐明。我们检查了水杨酸酯对3T3-L1脂肪细胞中几种脂肪因子和RAW 264.7细胞中LPS诱导的炎症因子的炎症相关变化的基因或蛋白质表达的影响。尤其是,我们将注意力集中在巨噬细胞和脂肪细胞之间的串扰上。暴露于RAW-CM培养基导致3T3-L1中TNF-α,IL-6和抵抗素的基因表达或蛋白质分泌增加,同时PPARγ和脂联素的基因表达减少脂肪细胞。水杨酸酯有效地逆转了这些变化,并上调了脂肪细胞中的葡萄糖消耗。我们还发现水杨酸抑制RAW-CM刺激的脂肪细胞中NF-κB的磷酸化。我们得出结论,水杨酸酯在炎症相关胰岛素抵抗的发病机理中阻断炎症过程。

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