Chondroitin sulfate and hyaluronic acid (500-730 kda) inhibit stromelysin-1 synthesis in human osteoarthritic chondrocytes.
Chondroitin sulfate and hyaluronic acid (500-730 kda) inhibit stromelysin-1 synthesis in human osteoarthritic chondrocytes.
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硫酸软骨素和透明质酸 (500-730 kda) 抑制人骨关节炎软骨细胞中基质溶素-1 的合成。
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
Pere Benito
中科院分区：
文献类型：
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作者：
Jordi Monfort;M. Nácher;E. Montell;J. Vila;J. Vergés;Pere Benito
硫酸软骨素（CS）和500-730 kDa透明质酸（HA）是治疗骨关节炎（OA）的症状性慢作用药物。此外，越来越多的证据表明CS和这种特异性HA作为OA过程的修饰剂的作用。CS和HA的治疗功效在于它们不同的作用机制。溶基质素-1（金属蛋白酶-3 [MMP-3]）是一种软骨蛋白水解酶，可诱导软骨破坏并充当炎症反应的介导剂。然而，很少有研究评估CS和HA对OA患者的人软骨细胞培养物中MMP-3合成的体外作用。因此，本研究的目的是分析CS和HA（500-730 kDa）对髋关节OA患者软骨细胞中白细胞介素-1 β（IL-1 β）诱导的MMP-3合成的影响。在不存在或存在不同HA 500-730 kDa（Hyalgan，Bioibérica Farma，Barcelona，Spain）浓度的情况下，将软骨细胞培养物与IL-1 β（2.5 ng/ml）孵育48 h，或者与浓度为10、50、100、150、200和1，000 μ g/ml的CS（Condro.san，Bioibérica Farma）孵育48 h。结果显示，CS和HA（500-730 kDa）均抑制IL-1 β诱导的人OA软骨细胞MMP-3的合成。具体地，CS和HA（500-730 kDa）在所有测试浓度下降低MMP-3表达水平。因此，我们的研究为这些药物的作用机制提供了新的数据，这可能有助于解释它们在OA患者中的临床疗效。
Chondroitin sulfate (CS) and 500-730 kDa hyaluronic acid (HA) are symptomatic slow-acting drugs for the treatment of osteoarthritis (OA). In addition, a growing body of evidence suggests a role for CS and this specific HA as modifiers of the course of OA. The therapeutic efficacy of CS and HA lies in their different mechanisms of action. Stromelysin-1 (metalloprotease-3 [MMP-3]) is a cartilage proteolytic enzyme, which induces cartilage destruction and acts as a mediator of the inflammatory response. However, there are few studies evaluating the in vitro effect of CS and HA on MMP-3 synthesis in human chondrocyte cultures from OA patients. Thus, the aim of the present study was to analyze the effect of CS and HA (500-730 kDa) on MMP-3 synthesis induced by interleukin-1beta (IL-1beta) in chondrocytes from patients with hip OA. Chondrocyte cultures were incubated for 48 h with IL-1beta (2.5 ng/ml) in the absence or presence of different HA 500-730 kDa (Hyalgan, Bioibérica Farma, Barcelona, Spain) concentrations, or alternatively, CS (Condro.san, Bioibérica Farma) at concentrations of 10, 50, 100, 150, 200 and 1,000 microg/ml. The results revealed that both CS and HA (500-730 kDa) inhibited MMP-3 synthesis induced by IL-1beta in human OA chondrocytes. Specifically, CS and HA (500-730 kDa) reduced MMP-3 expression levels at all tested concentrations. Therefore, our study provides new data on the mechanism of action of these drugs, which could help to explain their clinical efficacy in OA patients.