de Vries B J, van den Berg W B, Vitters E, van de Putte L B
J Rheumatol. 1986 Aug;13(4):686-93.
The established, suppressive effect of salicylate on sulfated glycosaminoglycan (sGAG) synthesis by normal articular cartilage was reinvestigated using anatomically intact articular cartilage of the whole mouse patella. Employing the physiological murine sulfate concentration (1.0 mM) sodium salicylate (1-5 X 10(-3) M) caused a dose dependent inhibition of 35S-sGAG synthesis (10-35%). At a lower sulfate concentration (0.4 mM) this inhibition was increased (15-45%) and the suppression was even more pronounced in sulfate deprived medium. This observation stresses the need of using physiological sulfate concentrations in cartilage culture studies. In the presence of 100% serum the therapeutic drug concentration (1-2 X 10(-3) M) had no longer any suppressive effect, either at 1.0 mM or at any lower sulfate concentration. Our data suggest that salicylate has no direct effect on sGAG metabolism in normal articular cartilage in vivo and that adverse effects may be due to the observed salicylate induced lowering of the endogenous sulfate level.
利用完整的小鼠髌骨关节软骨,对水杨酸盐对正常关节软骨硫酸化糖胺聚糖(sGAG)合成的既定抑制作用进行了重新研究。在生理浓度的鼠硫酸盐(1.0 mM)条件下,水杨酸钠(1 - 5×10⁻³ M)对³⁵S - sGAG合成产生剂量依赖性抑制(10 - 35%)。在较低的硫酸盐浓度(0.4 mM)下,这种抑制作用增强(15 - 45%),且在无硫酸盐培养基中抑制作用更为明显。该观察结果强调了在软骨培养研究中使用生理硫酸盐浓度的必要性。在含有100%血清的情况下,治疗药物浓度(1 - 2×10⁻³ M)在1.0 mM或任何较低的硫酸盐浓度下均不再具有抑制作用。我们的数据表明,水杨酸盐在体内对正常关节软骨的sGAG代谢没有直接影响,其不良反应可能是由于观察到的水杨酸盐诱导内源性硫酸盐水平降低所致。