Verschure P J, van der Kraan P M, Vitters E L, van den Berg W B
Department of Rheumatology, University Hospital Nijmegen, The Netherlands.
J Rheumatol. 1994 May;21(5):920-6.
During experimentally induced arthritis, inhibition of proteoglycan synthesis is one of the mechanisms leading to cartilage destruction. Disturbed anabolic signalling might contribute to this impaired chondrocyte proteoglycan synthesis. We investigated the effects of insulin-like growth factor 1 (IGF-1) and the glucocorticoid, triamcinolone acetonide, on in vitro chondrocyte proteoglycan synthesis of articular cartilage obtained from normal and arthritic mouse knee joints.
Proteoglycan synthesis was measured by 35S sulfate incorporation and the hydrodynamic volume of newly synthesized proteoglycans was analyzed with gel chromatography.
Culturing normal cartilage with IGF-1 resulted in significant enhancement of chondrocyte proteoglycan synthesis. Concerning the hydrodynamic volume of newly synthesized proteoglycans after culture with IGF-1, proteoglycan monomers with large hydrodynamic size, similar to those synthesized immediately after dissection were observed. In arthritic cartilage, IGF-1 failed to stimulate proteoglycan synthesis and only proteoglycans with relatively small dimensions were produced. However, in the presence of the steroid triamcinolone acetonide, synthesis of hydrodynamically large proteoglycans were found in arthritic as well as normal cartilage.
Our observations indicate that steroids may play a critical role in maintaining cartilage integrity in both normal and arthritic cartilage.
在实验性诱导的关节炎中，蛋白聚糖合成的抑制是导致软骨破坏的机制之一。合成代谢信号紊乱可能导致软骨细胞蛋白聚糖合成受损。我们研究了胰岛素样生长因子1（IGF-1）和糖皮质激素曲安奈德对从正常和患有关节炎的小鼠膝关节获取的关节软骨体外软骨细胞蛋白聚糖合成的影响。
通过35S硫酸盐掺入法测量蛋白聚糖合成，并使用凝胶色谱法分析新合成蛋白聚糖的流体动力学体积。
用IGF-1培养正常软骨导致软骨细胞蛋白聚糖合成显著增强。关于用IGF-1培养后新合成蛋白聚糖的流体动力学体积，观察到具有较大流体动力学尺寸的蛋白聚糖单体，类似于解剖后立即合成的那些。在患有关节炎的软骨中，IGF-1未能刺激蛋白聚糖合成，仅产生尺寸相对较小的蛋白聚糖。然而，在存在类固醇曲安奈德的情况下，在患有关节炎的软骨以及正常软骨中均发现了流体动力学尺寸较大的蛋白聚糖的合成。
我们的观察结果表明，类固醇可能在维持正常和患有关节炎的软骨中的软骨完整性方面发挥关键作用。
