Halliday D A, McNeil J D, Scicchitano R
Department of Medicine, Faculty of Medicine, University of Adelaide, Royal Adelaide Hospital, Australia.
Biochim Biophys Acta. 1992 Oct 6;1137(1):29-33. doi: 10.1016/0167-4889(92)90095-s.
Adult bovine articular chondrocytes were exposed to substance P, neurokinins A and B or substance P fragments, SP1-4, SP1-6 and SP7-11 in vitro. Proteoglycan synthesis was assessed by measuring proteoglycans which were released into the culture medium or incorporated into the cell layer. The intact tachykinins or substance P fragments had no direct effect on proteoglycan synthesis. Nor was total protein production affected. Gel chromatography, under dissociative conditions, revealed that sulphated proteoglycans detected in the medium or cell layer following treatment of chondrocytes with substance P, contained proteoglycans of similar molecular weight to those produced by cells exposed only to diluent controls. Therefore, we conclude that the acceleration of arthritis by substance P does not appear to be mediated through an effect on chondrocyte synthetic function.
将成年牛关节软骨细胞在体外暴露于P物质、神经激肽A和B或P物质片段,即SP1 - 4、SP1 - 6和SP7 - 11。通过测量释放到培养基中或整合到细胞层中的蛋白聚糖来评估蛋白聚糖的合成。完整的速激肽或P物质片段对蛋白聚糖合成没有直接影响。总蛋白产量也未受影响。在解离条件下进行的凝胶色谱分析表明,用P物质处理软骨细胞后,在培养基或细胞层中检测到的硫酸化蛋白聚糖所含蛋白聚糖的分子量与仅暴露于稀释剂对照的细胞所产生的蛋白聚糖相似。因此,我们得出结论,P物质加速关节炎的过程似乎不是通过对软骨细胞合成功能的影响来介导的。