Nietfeld J J, Wilbrink B, Den Otter W, Huber J, Huber-Bruning O
Department of Pathology, University Hospital Utrecht, The Netherlands.
J Rheumatol. 1990 Jun;17(6):818-26.
Human interleukin 1 (IL-1), up to 100 pg/ml, causes a decrease of the proteoglycan content of human (old and young) as well as porcine cartilage explants, without stimulating the proteoglycan release from the cartilage. The proteoglycan depletion is stronger in young than in old human cartilage and stronger in human than in porcine cartilage. The proteoglycan synthesis is considerably more inhibited by IL-1 in young than in old human cartilage. Our data suggest that an IL-1 induced inhibition of the proteoglycan synthesis, rather than a stimulation of proteoglycan breakdown causes the proteoglycan depletion of the cartilage. The data furthermore suggest a clear difference between young and old human cartilage, with respect to their sensitivity for IL-1. IL-1 in a concentration of 500 pg/ml causes in all 3 kinds of cartilage explants chondrocyte damage that might be relevant in the cartilage destruction during rheumatoid arthritis.
高达100 pg/ml的人白细胞介素1（IL-1）会导致人（年轻人和老年人）以及猪软骨外植体中蛋白聚糖含量降低，而不会刺激蛋白聚糖从软骨中释放。年轻人软骨中的蛋白聚糖耗竭比老年人软骨中的更强，人软骨中的比猪软骨中的更强。与老年人软骨相比，IL-1对年轻人软骨中蛋白聚糖合成的抑制作用明显更强。我们的数据表明，IL-1诱导的蛋白聚糖合成抑制而非蛋白聚糖分解刺激导致了软骨中蛋白聚糖的耗竭。此外，数据还表明年轻人和老年人软骨对IL-1的敏感性存在明显差异。浓度为500 pg/ml的IL-1会在所有3种软骨外植体中导致软骨细胞损伤，这可能与类风湿性关节炎期间的软骨破坏有关。
