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本文引用的文献

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Pharmacologic Therapies in Musculoskeletal Conditions.肌肉骨骼疾病的药物治疗
Med Clin North Am. 2016 Jul;100(4):869-90. doi: 10.1016/j.mcna.2016.03.015. Epub 2016 Apr 20.
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Ageing and the pathogenesis of osteoarthritis.衰老与骨关节炎的发病机制
Nat Rev Rheumatol. 2016 Jul;12(7):412-20. doi: 10.1038/nrrheum.2016.65. Epub 2016 May 19.
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Rutin protects rat articular chondrocytes against oxidative stress induced by hydrogen peroxide through SIRT1 activation.芦丁通过激活SIRT1保护大鼠关节软骨细胞免受过氧化氢诱导的氧化应激。
Biochem Biophys Res Commun. 2016 May 13;473(4):1301-1308. doi: 10.1016/j.bbrc.2016.04.064. Epub 2016 Apr 14.
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Chondroprotective effects of alpha-lipoic acid in a rat model of osteoarthritis.α-硫辛酸在骨关节炎大鼠模型中的软骨保护作用
Free Radic Res. 2016 Jul;50(7):767-80. doi: 10.1080/10715762.2016.1174775. Epub 2016 May 4.
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Molecular mechanisms and biomedical applications of glucosamine as a potential multifunctional therapeutic agent.氨基葡萄糖作为一种有潜力的多功能治疗药物的分子机制和生物医学应用。
Life Sci. 2016 May 1;152:21-9. doi: 10.1016/j.lfs.2016.03.028. Epub 2016 Mar 21.
6
Supplementation with α-Lipoic Acid Alone or in Combination with Eicosapentaenoic Acid Modulates the Inflammatory Status of Healthy Overweight or Obese Women Consuming an Energy-Restricted Diet.单独补充α-硫辛酸或与二十碳五烯酸联合补充可调节食用能量限制饮食的健康超重或肥胖女性的炎症状态。
J Nutr. 2015 Apr 1;146(4):889S-896S. doi: 10.3945/jn.115.224105.
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Biomarkers of (osteo)arthritis.(骨)关节炎的生物标志物。
Biomarkers. 2015;20(8):513-8. doi: 10.3109/1354750X.2016.1140930.
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ROS/oxidative stress signaling in osteoarthritis.骨关节炎中的ROS/氧化应激信号传导
Biochim Biophys Acta. 2016 Apr;1862(4):576-591. doi: 10.1016/j.bbadis.2016.01.003. Epub 2016 Jan 6.
9
Osteoarthritis year in review 2015: clinical.2015年骨关节炎年度回顾:临床篇
Osteoarthritis Cartilage. 2016 Jan;24(1):36-48. doi: 10.1016/j.joca.2015.07.026.
10
Osteoarthritis year in review 2015: mechanics.2015年骨关节炎年度回顾:力学
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α-硫辛酸增强鳄梨/大豆不皂化物在软骨细胞培养中的抗炎活性。

α-Lipoic Acid Potentiates the Anti-Inflammatory Activity of Avocado/Soybean Unsaponifiables in Chondrocyte Cultures.

作者信息

Frondoza Carmelita G, Fortuno Lowella V, Grzanna Mark W, Ownby Stacy L, Au Angela Y, Rashmir-Raven Ann M

机构信息

1 Nutramax Laboratories, Inc., Edgewood, MD, USA.

2 Department of Orthopaedic Surgery, Johns Hopkins University, Baltimore, MD, USA.

出版信息

Cartilage. 2018 Jul;9(3):304-312. doi: 10.1177/1947603516686146. Epub 2017 Jan 10.

DOI:10.1177/1947603516686146
PMID:29156944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6042030/
Abstract

Objective Pro-inflammatory mediators such as prostaglandin E-2 (PGE) play major roles in the pathogenesis of osteoarthritis (OA). Although current pharmacologic treatments reduce inflammation, their prolonged use is associated with deleterious side effects prompting the search for safer and effective alternative strategies. The present study evaluated whether chondrocyte production of PGE can be suppressed by the combination of avocado/soybean unsaponifiables (ASU) and α-lipoic acid (LA). Design Chondrocytes from articular cartilage of equine joints were incubated for 24 hours with: (1) control media, (2) ASU, (3) LA, or (4) ASU + LA combination. Cells were activated with lipopolysaccharide (LPS), interleukin 1β (IL-1β) or hydrogen peroxide (HO) for 24 hours and supernatants were immunoassayed for PGE. Nuclear factor-kappa B (NF-κB) analyses were performed by immunocytochemistry and Western blot following 1 hour of activation with IL-1β. Results LPS, IL-1β, or HO significantly increased PGE production. ASU or LA alone suppressed PGE production in LPS and IL-1β activated cells. Only LA alone at 2.5 µg/mL was inhibitory in HO-activated chondrocytes. ASU + LA inhibited more than either agent alone in all activated cells. ASU + LA also inhibited the IL-1β induced nuclear translocation of NF-κB. Conclusions The present study provides evidence that chondrocyte PGE production can be inhibited by the combination of ASU + LA more effectively than either ASU or LA alone. Inhibition of PGE production is associated with the suppression of NF-κB translocation. The potent inhibitory effect of ASU + LA on PGE production could offer a potential advantage for a combination anti-inflammatory/antioxidant approach in the management of OA.

摘要

目的 前列腺素E-2(PGE)等促炎介质在骨关节炎(OA)的发病机制中起主要作用。尽管目前的药物治疗可减轻炎症,但其长期使用会带来有害副作用,这促使人们寻找更安全有效的替代策略。本研究评估了鳄梨/大豆不皂化物(ASU)与α-硫辛酸(LA)联合使用是否能抑制软骨细胞产生PGE。

设计 将来自马关节软骨的软骨细胞与以下物质孵育24小时:(1)对照培养基,(2)ASU,(3)LA,或(4)ASU+LA组合。用脂多糖(LPS)、白细胞介素1β(IL-1β)或过氧化氢(HO)激活细胞24小时,然后对上清液进行PGE免疫测定。在用IL-1β激活1小时后,通过免疫细胞化学和蛋白质印迹法进行核因子-κB(NF-κB)分析。

结果 LPS、IL-1β或HO显著增加PGE的产生。单独使用ASU或LA可抑制LPS和IL-1β激活细胞中PGE的产生。仅2.5μg/mL浓度的LA单独使用时对HO激活的软骨细胞有抑制作用。在所有激活的细胞中,ASU+LA联合使用比单独使用任何一种药物的抑制作用更强。ASU+LA还抑制了IL-1β诱导的NF-κB核转位。

结论 本研究提供的证据表明,ASU+LA联合使用比单独使用ASU或LA更有效地抑制软骨细胞产生PGE。PGE产生受到抑制与NF-κB转位受到抑制有关。ASU+LA对PGE产生的强效抑制作用可能为OA管理中的联合抗炎/抗氧化方法提供潜在优势。