柳氮磺胺吡啶抑制白细胞介素-1β诱导的软骨细胞介导的降解。
Salazosulfapyridine suppresses chondrocyte mediated degradation induced by interleukin 1beta.
作者信息
Nose M, Sasano M, Kawashima Y
机构信息
Central Research Laboratories, Santen Pharmaceutical Co. Ltd., Osaka, Japan.
出版信息
J Rheumatol. 1997 Mar;24(3):550-4.
OBJECTIVE
To investigate the effects of salazosulfapyridine (SASP) and methotrexate (MTX) on interleukin (IL)-1beta treated rabbit chondrocytes.
METHODS
Normal rabbit chondrocytes were cultured to confluency. IL-1beta was added to serum-free culture medium in the presence or absence of SASP or MTX. After 2 days' incubation, the effects were evaluated from the responses of metalloproteinases, glycosaminoglycan (GAG), and prostaglandin E2 (PGE2).
RESULTS
SASP and MTX suppressed GAG and collagenase release into the culture medium from IL-1beta stimulated rabbit chondrocytes in a dose dependent manner. Only SASP suppressed stromelysin and PGE2 release.
CONCLUSION
SASP may have a protective effect on cartilage degradation of patients with rheumatoid arthritis.
目的
研究柳氮磺胺吡啶（SASP）和甲氨蝶呤（MTX）对白细胞介素（IL）-1β处理的兔软骨细胞的影响。
方法
将正常兔软骨细胞培养至汇合状态。在有或无SASP或MTX的情况下，将IL-1β添加到无血清培养基中。孵育2天后，从金属蛋白酶、糖胺聚糖（GAG）和前列腺素E2（PGE2）的反应来评估其效果。
结果
SASP和MTX以剂量依赖性方式抑制IL-1β刺激的兔软骨细胞向培养基中释放GAG和胶原酶。只有SASP抑制基质金属蛋白酶和PGE2的释放。
结论
SASP可能对类风湿性关节炎患者的软骨降解具有保护作用。
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