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白细胞介素-1在实验性关节炎软骨破坏中起关键作用的体内证据。

In vivo evidence for a key role of IL-1 in cartilage destruction in experimental arthritis.

作者信息

van den Berg W B, van de Loo F A, Otterness I, Arntz O, Joosten L A

机构信息

Dept of Rheumatology, University Hospital Nijmegen, The Netherlands.

出版信息

Agents Actions Suppl. 1991;32:159-63. doi: 10.1007/978-3-0348-7405-2_21.

Abstract

Cartilage destruction in murine antigen induced arthritis is characterized by enhanced degradation of proteoglycans and inhibition of chondrocyte proteoglycan synthesis. Within this model common NSAIDs only suppress joint swelling, and to some extent granulocyte infiltration, but leave the process of cartilage destruction undisturbed. Evidence is now accumulating that the vast amount of activated granulocytes in the joint space are of minor importance, and that interleukin-1 (IL-1) is the key mediator in this process. Treatment of mice with neutralizing antibodies against IL-1 resulted in relief of chondrocyte proteoglycan synthesis inhibition and prevented matrix destruction. This indicates that it makes sense to focus future therapy on elimination of IL-1.

摘要

小鼠抗原诱导性关节炎中的软骨破坏表现为蛋白聚糖降解增强以及软骨细胞蛋白聚糖合成受到抑制。在该模型中,常见的非甾体抗炎药仅能抑制关节肿胀,在一定程度上抑制粒细胞浸润,但对软骨破坏过程并无影响。目前越来越多的证据表明,关节腔内大量活化的粒细胞作用较小,而白细胞介素-1(IL-1)是这一过程中的关键介质。用抗IL-1中和抗体治疗小鼠可缓解软骨细胞蛋白聚糖合成抑制,并防止基质破坏。这表明未来将治疗重点放在消除IL-1上是有意义的。

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