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首页> 外文期刊>Journal of medicinal food >Avocado/Soybean Unsaponifiables, Glucosamine and Chondroitin Sulfate Combination Inhibits Proinflammatory COX-2 Expression and Prostaglandin E2 Production in Tendon-Derived Cells
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Avocado/Soybean Unsaponifiables, Glucosamine and Chondroitin Sulfate Combination Inhibits Proinflammatory COX-2 Expression and Prostaglandin E2 Production in Tendon-Derived Cells

机译:鳄梨/大豆未加工,氨基葡萄糖和软骨素组合抑制肌腱衍生细胞中的促炎核心COX-2表达和前列腺素E2产生

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摘要

Tendinopathy, a common disorder in man and horses, is characterized by pain, dysfunction, and tendon degeneration. Inflammation plays a key role in the pathogenesis of tendinopathy. Tendon cells produce proinflammatory molecules that induce pain and tissue deterioration. Currently used nonsteroidal anti-inflammatory drugs are palliative but have been associated with adverse side effects prompting the search for safe, alternative compounds. This study determined whether tendon-derived cells' expression of proinflammatory cyclooxygenase (COX)-2 and production of prostaglandin E2 (PGE(2)) could be attenuated by the combination of avocado/soybean unsaponifiables (ASU), glucosamine (GLU), and chondroitin sulfate (CS). ASU, GLU, and CS have been used in the management of osteoarthritis-associated joint inflammation. Tenocytes in monolayer and microcarrier spinner cultures were incubated with media alone, or with the combination of ASU (8.3 mu g/mL), GLU (11 mu g/mL), and CS (20 mu g/mL). Cultures were next incubated with media alone, or stimulated with interleukin-1 beta (IL-1 beta; 10 ng/mL) for 1 h to measure COX-2 gene expression, or for 24 h to measure PGE(2) production, respectively. Tenocyte phenotype was analyzed by phase-contrast microscopy, immunocytochemistry, and Western blotting. Tendon-derived cells proliferated and produced extracellular matrix component type I collagen in monolayer and microcarrier spinner cultures. IL-1 beta-induced COX-2 gene expression and PGE(2) production were significantly reduced by the combination of (ASU+GLU+CS). The suppression of IL-1 beta-induced inflammatory response suggests that (ASU+GLU+CS) may help attenuate deleterious inflammation in tendons.
机译:肌腱病变,男人和马的常见疾病,其特征在于疼痛,功能障碍和肌腱变性。炎症在肌腱病的发病机制中起着关键作用。肌腱细胞产生诱导疼痛和组织劣化的促炎分子。目前使用的非甾体抗炎药是姑息性的,但已经与促进寻求安全,替代化合物的不利副作用有关。该研究确定了肌腱衍生的细胞的促炎环氧酶(COX)-2的表达和前列腺素E2的产生(PGE(2))可以通过鳄梨/大豆未加工(ASU),葡糖胺(Glu)的组合来衰减硫酸软骨素(CS)。 ASU,Glu和CS已被用于骨关节炎相关关节炎症的管理。单层和微括号旋转器培养物中的胞粒细胞单独孵育,或者用ASU(8.3μg/ ml),glu(11μg/ ml)和Cs(20μg/ ml)的组合一起温育。接下来将培养物单独孵育培养基,或用白细胞介素-1β(IL-1β; 10ng / ml)刺激1小时以测量COX-2基因表达,或24小时分别测量PGE(2)生产。通过相位对比显微镜,免疫细胞化学和蛋白质印迹分析了替尼蛋白表型。肌腱衍生的细胞增殖和产生的细胞外基质组分I型胶原蛋白在单层和微载体旋转器培养物中。通过(ASU + Glu + Cs)的组合显着降低了IL-1β诱导的COX-2基因表达和PGE(2)产生。抑制IL-1β诱导的炎症反应表明(ASU + Glu + Cs)可能有助于衰减肌腱中的有害炎症。

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