Chondrocyte Production of Pro-Inflammatory Chemokine MCP-1 (CCL-2) and Prostaglandin E-2 Is Inhibited by Avocado/Soybean Unsaponifiables, Glucosamine, Chondroitin Sulfate Combination

E. Secor, M. Grzanna, A. Rashmir-Raven, C. Frondoza
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引用次数: 4

Abstract

Osteoarthritis (OA) is a chronic, painful disease affecting articulating joints in man and animals. It is characterized by cartilage breakdown, bone remodeling, osteophyte formation and joint inflammation. Currently used non-steroidal anti-inflammatory drugs for the management of OA are known to have deleterious side effects. To address the need for alternatives, we evaluated the anti-inflammatory effects of a combination of avocado/soybean unsaponifiables (ASU), glucosamine (GLU) and chondroitin sulfate (CS) by measuring chemokine MCP-1 (monocyte chemoattractant protein 1, CCL2) and prostaglandin E-2 (PGE2) in stimulated chondrocytes. As the only cellular constituents of cartilage, chondrocytes are the source of pro-inflammatory mediators that play critical roles in the pathogenesis of OA. Chondrocytes were incubated: with: 1) control media, 2) [ASU + GLU + CS] combination, or 3) Phenylbutazone (PBZ) for 24 hours. Cells were next stimulated with IL-1β or LPS for another 24 hrs. MCP-1 and PGE2 from supernatants were quantitated by immunoassay. Another set of chondrocytes seeded in chamber slides were stimulated with IL-1β for 1 hour and then immunostained for NF-κB. Chondrocytes stimulated with IL-1β or LPS significantly increased MCP-1 and PGE2 production which were significantly reduced after treatment with [ASU + GLU + CS]. In contrast, PBZ significantly reduced PGE2 but not MCP-1 production. IL-1β stimulation induced nuclear translocation of NF-κB, which was inhibited by pre-treatment with either [ASU + GLU + CS] or PBZ. The present study provides evidence that the production of MCP-1 by chondrocytes can be inhibited by the combination of [ASU + GLU + CS] but not by PBZ. In contrast, PGE2 production was inhibited by either treatment suggesting that the production of MCP-1 and PGE2 could be independently regulated. The finding of distinct effects of [ASU + GLU + CS] on MCP-1 and PGE2 synthesis supports a scientific rationale for a multimodal treatment approach in the management of OA.
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鳄梨/大豆不皂化物、葡萄糖胺、硫酸软骨素联合抑制促炎趋化因子MCP-1 (CCL-2)和前列腺素E-2的软骨细胞生成
骨关节炎(OA)是一种影响人类和动物关节的慢性疼痛疾病。它的特点是软骨破裂,骨重塑,骨赘形成和关节炎症。目前用于OA治疗的非甾体抗炎药已知具有有害的副作用。为了解决替代品的需求,我们通过测量受刺激软骨细胞中的趋化因子MCP-1(单核细胞趋化蛋白1,CCL2)和前列腺素E-2 (PGE2)来评估鳄梨/大豆不皂甙(ASU)、葡萄糖胺(GLU)和硫酸软骨素(CS)的组合的抗炎作用。作为软骨的唯一细胞成分,软骨细胞是促炎介质的来源,在OA的发病机制中起关键作用。软骨细胞孵育:1)对照培养基,2)[ASU + GLU + CS]组合,或3)苯丁酮(PBZ)孵育24小时。然后用IL-1β或LPS刺激细胞24小时。免疫法测定上清液中MCP-1和PGE2的含量。另一组软骨细胞接种于载玻片中,IL-1β刺激1小时,然后进行NF-κB免疫染色。IL-1β或LPS刺激软骨细胞显著增加MCP-1和PGE2的产生,而ASU + GLU + CS治疗后MCP-1和PGE2的产生显著降低。相比之下,PBZ显著降低了PGE2的产生,但没有降低MCP-1的产生。IL-1β刺激可诱导NF-κB核易位,[ASU + GLU + CS]或PBZ预处理可抑制NF-κB核易位。本研究提供的证据表明,[ASU + GLU + CS]可以抑制软骨细胞产生MCP-1,但PBZ不能。相比之下,两种处理均抑制PGE2的产生,这表明MCP-1和PGE2的产生可以独立调节。[ASU + GLU + CS]对MCP-1和PGE2合成的不同影响的发现为OA管理中采用多模式治疗方法提供了科学依据。
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