Bassleer C T, Combal J P, Bougaret S, Malaise M
Laboratory of Rheumatology, University of Liège, Belgium.
Osteoarthritis Cartilage. 1998 May;6(3):196-204. doi: 10.1053/joca.1998.0112.
To test the effects of chondroitin sulfate (ACS, a glycosaminoglycan of cartilage) with and without interleukin-1 beta (IL-1 beta) on human articular chondrocytes cultivated in clusters and in long-term (0-16 days or 16-32 days).
Chondrocyte productions of proteoglycans (PGs), type II collagen (coll-II) and prostaglandin E2 (PGE2) were assayed by specific radioimmunoassays applied to conditioned culture media and to clusters.
During the two culture periods (0-16 days or 16-32 days), ACS (100-1000 micrograms/ml) increased total PG production and had no effect on the production of coll-II by chondrocytes. During the first 16 days, ACS (500-1000 micrograms/ml) decreased total PGE2 synthesis. IL-1 beta decreased PG and coll-II productions and increased PGE2 synthesis. During the first period (0-16 days), while the cluster is forming, ACS counteracted the IL-1 beta-induced effects on PG (500-1000 micrograms ACS/ml), coll-II (100-1000 micrograms ACS/ml) and PGE2 (500-1000 micrograms ACS/ml) productions. During the second period (16-32 days), when the cluster is already formed, ACS counteracted the IL-1 beta-induced effects on total PG (100-1000 micrograms ACS/ml), coll-II (1000 micrograms ACS/ml) and PGE2 (1000 micrograms ACS/ml) productions.
These in vitro studies suggest that ACS is able to increase matrix component production by human chondrocytes and to inhibit the negative effects of IL-1 beta.
测试硫酸软骨素(ACS,一种软骨糖胺聚糖)在有和没有白细胞介素-1β(IL-1β)的情况下,对成簇培养和长期培养(0 - 16天或16 - 32天)的人关节软骨细胞的影响。
通过应用于条件培养基和成簇细胞的特异性放射免疫测定法,检测蛋白聚糖(PGs)、II型胶原蛋白(coll-II)和前列腺素E2(PGE2)的软骨细胞生成量。
在两个培养阶段(0 - 16天或16 - 32天),ACS(100 - 1000微克/毫升)增加了总PG生成量,且对软骨细胞的coll-II生成量没有影响。在最初的16天里,ACS(500 - 1000微克/毫升)降低了总PGE2合成。IL-1β降低了PG和coll-II生成量,并增加了PGE2合成。在第一阶段(0 - 16天),当细胞簇形成时,ACS抵消了IL-1β对PG(500 - 1000微克ACS/毫升)、coll-II(100 - 1000微克ACS/毫升)和PGE2(500 - 1000微克ACS/毫升)生成的诱导作用。在第二阶段(16 - 32天),当细胞簇已经形成时,ACS抵消了IL-1β对总PG(100 - 1000微克ACS/毫升)、coll-II(1000微克ACS/毫升)和PGE2(1000微克ACS/毫升)生成的诱导作用。
这些体外研究表明,ACS能够增加人软骨细胞的基质成分生成,并抑制IL-1β的负面影响。