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首页> 外文期刊>Journal of Cellular Physiology >Possible Involvement of Palmitate in Pathogenesis of Periodontitis
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Possible Involvement of Palmitate in Pathogenesis of Periodontitis

机译：棕榈酸酯参与发病机理牙周炎的

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Type 2 diabetes (T2D) is characterized by decreased insulin sensitivity and higher concentrations of free fatty acids (FFAs) in plasma. Among FFAs, saturated fatty acids (SFAs), such as palmitate, have been suggested to promote inflammatory responses. Although many epidemiological studies have shown a link between periodontitis and T2D, little is known about the clinical significance of SFAs in periodontitis. In this study, we showed that gingival fibroblasts have cell-surface expression of CD36, which is also known as FAT/fatty acid translocase. Moreover, CD36 expression was increased in gingival fibroblasts of high-fat diet-induced T2D model mice, compared with gingival fibroblasts of mice fed a normal diet. DNA microarray analysis revealed that palmitate increased mRNA expression of pro-inflammatory cytokines and chemokines in human gingival fibroblasts (HGF). Consistent with these results, we confirmed that palmitate-induced interleukin (IL)-6, IL-8, and CXCL1 secretion in HGF, using a cytokine array and ELISA. SFAs, but not an unsaturated fatty acid, oleate, induced IL-8 production. Docosahexaenoic acid (DHA), which is one of the omega-3 polyunsaturated fatty acids, significantly suppressed palmitate-induced IL-6 and IL-8 production. Treatment of HGF with a CD36 inhibitor also inhibited palmitate-induced pro-inflammatory responses. Finally, we demonstrated that Porphyromonas gingivalis (P.g.) lipopolysaccharide and heat-killed P.g. augmented palmitate-induced chemokine secretion in HGF. These results suggest a potential link between SFAs in plasma and the pathogenesis of periodontitis. (C) 2015 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.
机译：2型糖尿病(T2D)的特点是降低胰岛素敏感性和高游离脂肪酸的浓度(远期运费协议)等离子体。棕榈酸酯等,建议推广炎症反应。流行病学研究显示之间的联系牙周炎和T2D,知之甚微美国在牙周炎的临床意义。在这项研究中,我们表明,牙龈成纤维细胞细胞表面CD36的表达,这也被称为脂肪/脂肪酸移位酶。牙龈成纤维细胞的脂肪增加食源性T2D模型小鼠,相比之下牙龈成纤维细胞的正常饮食的老鼠。DNA微阵列分析表明,棕榈酸酯增加促炎的mRNA的表达细胞因子和趋化因子在人类牙龈成纤维细胞(HGF)。我们确认palmitate-induced白介素(IL) 6、引发和处于分泌HGF的使用细胞因子和ELISA数组。不饱和脂肪酸、油酸诱导引发生产。ω- 3多不饱和脂肪酸,显著抑制palmitate-induced il - 6和引发生产。抑制剂也抑制palmitate-induced炎性反应。证明Porphyromonas gingivalis(供货商)。脂多糖和heat-killed P.g.增强HGF palmitate-induced趋化因子的分泌。这些结果表明潜在的联系美国在等离子体和发病机理牙周炎。细胞生理由威利出版期刊、公司。

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