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首页> 外文期刊>International journal of molecular medicine >The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells
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The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

机译:乳脑膜下裸球菌的正丁醇部分通过下调人内皮细胞中NF-κB抑制炎症反应

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Naematoloma sublateritium (Fr.) P. Karst is a chestnut mushroom that is currently a popular edible fungus in the USA, Japan, China and Korea. Although its therapeutic potential in the treatment of diseases has been demonstrated, the pharmacological effect of N.?sublateritium (NS) has been poorly studied. In the present study, we demonstrate for the first time that NS suppresses TNF-α-induced inflammatory response in human umbilical vein endothelial cells. The n-butanol fraction of NS (BFNS) inhibited TNF-α-induced monocyte adhesion to endothelial cells in a dose-dependent manner. The anti-adhesive activity of BFNS correlated with suppressed expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, monocyte chemoattractant protein-1 and interleukin-8 at both the mRNA and protein levels. In addition, BFNS dose-dependently decreased the expression of inducible nitrogen oxygen synthase (iNOS) and cyclooxygenase-2 (COX-2). Notably, BFNS significantly regulated the nuclear factor (NF)-κB transcriptional activity that was activated by TNF-α stimulation. When considered together, these results suggest that BFNS inhibits the expression of TNF-α-induced adhesion molecules in addition to regulating the iNOS/COX-2 pathways through the modulation of NF-κB in endothelial cells. In conclusion, we propose that BFNS may be a potential therapeutic agent against vascular inflammation, such as atherosclerosis.
机译:Suberitritium(Fr.)Naematoloma sublateritium(Fr.)Karst是一种栗子蘑菇,目前在美国,日本,中国和韩国是一种受欢迎的食用菌。尽管已经证明了其在疾病治疗中的治疗潜力,但是对亚硫酸盐亚铁盐(NS)的药理作用却研究不足。在本研究中,我们首次证明了NS抑制TNF-α诱导的人脐静脉内皮细胞的炎症反应。 NS的正丁醇部分(BFNS)以剂量依赖的方式抑制TNF-α诱导的单核细胞粘附于内皮细胞。 BFNS的抗粘附活性与在mRNA和蛋白质水平上抑制的血管细胞粘附分子-1,细胞间粘附分子-1,单核细胞趋化蛋白1和白细胞介素8的表达有关。此外,BFNS剂量依赖性地降低了诱导型氮氧合酶(iNOS)和环氧合酶2(COX-2)的表达。值得注意的是,BFNS显着调节了由TNF-α刺激激活的核因子(NF)-κB转录活性。综合考虑,这些结果表明,BFNS除了通过调节内皮细胞中的NF-κB调节iNOS / COX-2途径外,还抑制TNF-α诱导的粘附分子的表达。总之,我们建议BFNS可能是对抗血管炎症(如动脉粥样硬化)的潜在治疗剂。

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