Kandel R A, Petelycky M, Dinarello C A, Minden M, Pritzker K P, Cruz T F
Department of Pathology, Mt. Sinai Hospital, Toronto, ON, Canada.
J Rheumatol. 1990 Jul;17(7):953-7.
In order to determine whether interleukin 6 (IL-6) is involved in the pathogenesis of the cartilage destruction observed in arthritis, the effect of human recombinant IL-6 on collagenase production and proteoglycan synthesis by bovine articular chondrocytes was examined. Addition of IL-6 (1.0 to 1000 U/ml) to the culture medium did not stimulate collagenase production or alter proteoglycan secretion. Whereas human purified interleukin 1 (IL-1) (20 U/ml) stimulated collagenase production and inhibited proteoglycan synthesis. Furthermore addition of IL-1 (20 U/ml) to chondrocyte cultures did not stimulate the chondrocytes to produce IL-6. Under our experimental conditions, IL-6 did not stimulate chondrocytes to proliferate as measured by [3H] thymidine incorporation. This would suggest that IL-6 is not involved in mediating cartilage loss.
为了确定白细胞介素6(IL-6)是否参与关节炎中观察到的软骨破坏的发病机制,研究了重组人IL-6对牛关节软骨细胞胶原酶产生和蛋白聚糖合成的影响。向培养基中添加IL-6(1.0至1000 U/ml)不会刺激胶原酶产生或改变蛋白聚糖分泌。而人纯化白细胞介素1(IL-1)(20 U/ml)可刺激胶原酶产生并抑制蛋白聚糖合成。此外,向软骨细胞培养物中添加IL-1(20 U/ml)不会刺激软骨细胞产生IL-6。在我们的实验条件下,通过[3H]胸苷掺入法测定,IL-6不会刺激软骨细胞增殖。这表明IL-6不参与介导软骨损伤。