首页> 外文期刊>The Journal of Nutritional Biochemistry >Linoleic acid increases monocyte chemotaxis and adhesion to human aortic endothelial cells through protein kinase C- and cyclooxygenase-2-dependent mechanisms.
【24h】

Linoleic acid increases monocyte chemotaxis and adhesion to human aortic endothelial cells through protein kinase C- and cyclooxygenase-2-dependent mechanisms.

机译:亚油酸通过蛋白激酶C和环加氧酶2依赖性机制增强单核细胞趋化性和对人主动脉内皮细胞的粘附。

获取原文
获取原文并翻译 | 示例
       

摘要

The effects of polyunsaturated n-6 linoleic acid on monocyte-endothelial interactions were investigated with particular emphasis on the expression of platelet/endothelial cell adhesion molecule (PECAM)-1 and the role of protein kinase C (PKC) and cyclooxygenase-2 (COX-2). As a diet rich in polyunsaturated fatty acids may favour atherosclerosis in hyperglycaemia, this study was performed in both normal and high-glucose media using human aortic endothelial cells (HAEC). The HAEC were preincubated with normal (5 mM) or high (25 mM) D-glucose for 3 days before addition of fatty acids (0.2 mM) for 3 days. Linoleic acid enhanced PECAM-1 expression independently of tumor necrosis factor (TNF)-alpha and significantly increased TNF-alpha-induced monocyte adhesion to HAEC in comparison to the monounsaturated n-9 oleic acid. Chronic glucose treatment (25 mM, 6 days) did not modify the TNF-alpha-induced or fatty acid-induced changes in monocyte binding. The increase in monocyte binding was accompanied by a significant increase in E-selectin and vascular cell adhesion molecule (VCAM)-1 expression and could be abrogated by an interleukin (IL)-8 neutralising antibody and by the PKC and COX inhibitors. Inhibition of PKC-delta reduced VCAM-1 expression regardless of experimental condition and was accompanied by a significant decrease in monocyte binding. Conditioned medium from linoleic acid-treated HAEC grown in normal glucose conditions significantly increased THP-1 chemotaxis. These results suggest that linoleic acid-induced changes in monocyte chemotaxis and subsequent binding are not solely mediated by changes in adhesion molecule expression but may be due to secreted factors such as IL-8, monocyte chemoattractant protein-1 or prostaglandins (PGs) such as PGE(2), as IL-8 neutralisation and COX-2 inhibition reduced monocyte binding without changes in adhesion molecule expression
机译:研究了多不饱和n-6亚油酸对单核细胞与内皮细胞相互作用的影响,尤其着重于血小板/内皮细胞粘附分子(PECAM)-1的表达以及蛋白激酶C(PKC)和环氧合酶2(COX)的作用-2)。由于富含多不饱和脂肪酸的饮食可能在高血糖症中促进动脉粥样硬化,因此这项研究是在正常和高葡萄糖培养基中使用人主动脉内皮细胞(HAEC)进行的。将HAEC与正常(5 mM)或高(25 mM)D-葡萄糖预孵育3天,然后添加脂肪酸(0.2 mM)3天。与单不饱和n-9油酸相比,亚油酸独立于肿瘤坏死因子(TNF)-α增强了PECAM-1的表达,并显着增加了TNF-α诱导的单核细胞对HAEC的粘附。慢性葡萄糖治疗(25 mM,6天)未改变TNF-α诱导或脂肪酸诱导的单核细胞结合变化。单核细胞结合的增加伴随着E-选择素和血管细胞粘附分子(VCAM)-1的表达显着增加,并且可以被白介素(IL)-8中和抗体以及PKC和COX抑制剂所消除。不论实验条件如何,抑制PKC-δ都会降低VCAM-1表达,并伴有单核细胞结合的显着降低。在正常葡萄糖条件下生长的亚油酸处理过的HAEC的条件培养基显着提高了THP-1的趋化性。这些结果表明,亚油酸诱导的单核细胞趋化性和随后的结合变化不仅是由粘附分子表达的变化介导的,而且可能是由于诸如IL-8,单核细胞趋化蛋白1或前列腺素(PGs)等分泌因子引起的。 PGE(2),因为IL-8中和和COX-2抑制作用减少了单核细胞结合,而粘附分子表达没有变化

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号