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白细胞介素-1对小鼠造成轻度关节炎损伤后关节软骨中蛋白聚糖的丢失及随后的补充:恢复期蛋白聚糖周转受损。

Proteoglycan loss and subsequent replenishment in articular cartilage after a mild arthritic insult by IL-1 in mice: impaired proteoglycan turnover in the recovery phase.

作者信息

van de Loo A A, Arntz O J, Otterness I G, van den Berg W B

机构信息

Department of Rheumatology, University Hospital Nijmegen, The Netherlands.

出版信息

Agents Actions. 1994 May;41(3-4):200-8. doi: 10.1007/BF02001917.

Abstract

The reparative responses of articular cartilage after an arthritic insult have not been studied extensively to this day. In the present study, we injected interleukin-1 (IL-1) into knee joints of mice to provoke a mild and transient arthritic insult, and characterized both the catabolic and the subsequent recovery phase. In the catabolic phase, which lasted 2 days after IL-1 injection, proteoglycan (PG) breakdown was profoundly accelerated and PG synthesis was markedly inhibited. Sulfation and polysaccharide synthesis were not affected, yet the number of chondroitin sulfate chains was decreased. The general chondrocyte protein synthesis was not inhibited by IL-1. IL-1 injected every other day for a total of three injections prolonged this catabolic phase and resulted in frank loss of articular cartilage proteoglycans. In the recovery phase, started 3 days after IL-1, PG synthesis was enhanced (1.7 times the normal) and proteoglycans had normal hydrodynamic properties. Remarkably, PG degradation was significantly decreased (approximately 50% of the normal). Zymographic analysis demonstrated enhanced expression of gelatinolytic activities in the extracts of the articular tissues shortly after IL-1 exposure and decreased levels in the recovery phase. We found that the overshoot of PG synthesis and impaired degradation act together to facilitate full cartilage repair 7 days after the last of the three IL-1 injections.

摘要

迄今为止,尚未对关节炎损伤后关节软骨的修复反应进行广泛研究。在本研究中,我们向小鼠膝关节注射白细胞介素-1(IL-1)以引发轻度短暂的关节炎损伤,并对分解代谢阶段和随后的恢复阶段进行了表征。在分解代谢阶段,即IL-1注射后持续2天,蛋白聚糖(PG)分解显著加速,PG合成明显受到抑制。硫酸化和多糖合成未受影响,但硫酸软骨素链的数量减少。一般软骨细胞蛋白合成未被IL-1抑制。每隔一天注射一次IL-1,共注射三次,延长了这个分解代谢阶段,并导致关节软骨蛋白聚糖明显丢失。在恢复阶段,即IL-1注射3天后开始,PG合成增强(为正常水平的1.7倍),蛋白聚糖具有正常的流体动力学特性。值得注意的是,PG降解显著降低(约为正常水平的50%)。酶谱分析表明,IL-1暴露后不久,关节组织提取物中的明胶酶活性表达增强,而在恢复阶段水平降低。我们发现,PG合成的过度增加和降解受损共同作用,促进了三次IL-1注射中的最后一次注射7天后软骨的完全修复。

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