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首页> 外文期刊>The Journal of Nutritional Biochemistry >Altered NF-kappaB gene expression and collagen formation induced by polyunsaturated fatty acids
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Altered NF-kappaB gene expression and collagen formation induced by polyunsaturated fatty acids

机译：多不饱和脂肪酸诱导的NF-κB基因表达改变和胶原形成

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Inability to control collagen formation in vital organs (e.g., fibrosis) or stimulate healthy collagen production (CP) in connective tissues (e.g., ligaments) is a major cause of death and disability. This study tested the hypothesis that arachidonicacid (AA) and eicosapentaenoic acid (EPA) influenced CP in 3T3-Swiss fibroblasts by altering gene expression in the nuclear factor-kappa B (NF-kappaB) pathway. 3T3-Swiss fibroblasts were grown in medium containing either AA or EPA. Lipopolysaccharide (LPS) was used to activate NF-kappaB, and parthenolide was used to block it. Cells treated with EPA had increased expression of genes in the NF-kappaB pathway when exposed to LPS and also produced more collagen. Parthenolide blocked NF-kappaB activation toa greater extent in EPA-treated cells and also decreased CP induced by NF-kappaB activation. Genes in the NF-kappaB signaling pathway that had increased expression in EPA-treated cells included the toll-like receptor 4 (Tlr4), adaptor proteins [TNF receptor-associated factor 6 (Traf6), myeloid differentiation primary response gene 88], signal transduction kinases (NF-kappaB-inducing kinase, inhibitors of kappa light polypeptide gene enhancer isoforms), inhibitor protein (I-KB alpha chain), transcriptionfactors (nuclear factor of kappa light chain gene enhancer, p105 and NF-kappaB subunit p100), DNA binding proteins (cAMP response element binding protein) and response genes known to affect CP [interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), monocyte chemotactic protein-1]. This study raises the possibility that fatty acids may be used as adjuvants in combination with other therapies (e.g., selective targeting of the NF-kappaB pathway) to control collagen formation.
机译：无法控制重要器官中胶原蛋白的形成（例如纤维化）或不能刺激结缔组织（例如韧带）中健康的胶原蛋白产生（CP）是死亡和残疾的主要原因。这项研究验证了花生四烯酸（AA）和二十碳五烯酸（EPA）通过改变核因子-κB（NF-kappaB）途径中的基因表达影响3T3-瑞士成纤维细胞中CP的假设。 3T3-Swiss成纤维细胞在含有AA或EPA的培养基中生长。脂多糖（LPS）用于激活NF-κB，而小白菊内酯用于阻断它。当暴露于LPS时，用EPA处理的细胞在NF-κB通路中的基因表达增加，并且还产生更多的胶原蛋白。偏苯二酚在EPA处理的细胞中更大程度地阻断了NF-κB的活化，并且还降低了由NF-κB活化诱导的CP。在EPA处理的细胞中表达增加的NF-κB信号通路中的基因包括toll样受体4（Tlr4），衔接蛋白[TNF受体相关因子6（Traf6），髓样分化主要反应基因88]，信号转导激酶（NF-κB诱导激酶，κ轻型多肽基因增强子异构体的抑制剂），抑制剂蛋白（I-KBα链），转录因子（κ轻型基因增强子的核因子，p105和NF-kappaB亚基p100）， DNA结合蛋白（cAMP反应元件结合蛋白）和已知影响CP的反应基因[白介素6（IL-6），诱导型一氧化氮合酶（iNOS），单核细胞趋化蛋白-1]。这项研究提出了脂肪酸可以与其他疗法（例如，选择性靶向NF-κB途径）结合使用作为佐剂来控制胶原蛋白形成的可能性。

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