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首页> 外文期刊>Matrix biology: Journal of the International Society for Matrix Biology >Selective and non-selective metalloproteinase inhibitors reduce IL-1-induced cartilage degradation and loss of mechanical properties.
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Selective and non-selective metalloproteinase inhibitors reduce IL-1-induced cartilage degradation and loss of mechanical properties.

机译：选择性和非选择性金属蛋白酶抑制剂可减少IL-1诱导的软骨降解和机械性能丧失。

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摘要

Articular cartilage undergoes matrix degradation and loss of mechanical properties when stimulated with proinflammatory cytokines such as interleukin-1 (IL-1). Aggrecanases and matrix metalloproteinases (MMPs) are thought to be principal downstream effectors of cytokine-induced matrix catabolism, and aggrecanase- or MMP-selective inhibitors reduce or block matrix destruction in several model systems. The objective of this study was to use metalloproteinase inhibitors to perturb IL-1-induced matrix catabolism in bovine cartilage explants and examine their effects on changes in tissue compression and shear properties. Explanted tissue was stimulated with IL-1 for up to 24 days in the absence or presence of inhibitors that were aggrecanase-selective, MMP-selective, or non-selective. Analysis of conditioned media and explant digests revealed that aggrecanase-mediated aggrecanolysis was delayed to varying extents with all inhibitor treatments, but that aggrecan release persisted. Collagen degradation was abrogated by MMP- and non-selective inhibitors and reduced by the aggrecanase inhibitor. The inhibitors delayed but did not reduce loss of the equilibrium compression modulus, whereas the losses of dynamic compression and shear moduli were delayed and reduced. The data suggest that non-metalloproteinase mechanisms participate in IL-1-induced matrix degradation and loss of tissue material properties.
机译：当用促炎细胞因子如白细胞介素-1（IL-1）刺激时，关节软骨会经历基质降解和机械性能下降。 Aggrecanases和基质金属蛋白酶（MMP）被认为是细胞因子诱导的基质分解代谢的主要下游效应物，在几种模型系统中，聚集蛋白聚糖酶或MMP选择性抑制剂可减少或阻断基质破坏。这项研究的目的是使用金属蛋白酶抑制剂干扰牛软骨外植体中IL-1诱导的基质分解代谢，并研究它们对组织压缩和剪切特性变化的影响。在不存在或存在聚集蛋白聚糖酶选择性，MMP选择性或非选择性抑制剂的情况下，用IL-1刺激移植的组织长达24天。条件培养基和外植体消化物的分析显示，在所有抑制剂处理下，软骨聚集蛋白聚糖酶介导的软骨聚集蛋白水解作用均在不同程度上延迟，但聚集蛋白聚糖的释放持续。 MMP和非选择性抑制剂可消除胶原蛋白降解，而聚集蛋白聚糖酶抑制剂可减少胶原蛋白降解。阻滞剂延迟但不降低平衡压缩模量的损失，而动态压缩和剪切模量的损失被延迟并减少。数据表明非金属蛋白酶机制参与IL-1诱导的基质降解和组织材料特性的丧失。

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