[病情缓解抗风湿药物（DMARDs）和地塞米松（DEX）对白细胞介素-1β（IL-1β）刺激的滑膜培养细胞产生白细胞介素-1β和白细胞介素-6的影响]
[Effects of disease modifying antirheumatic drugs (DMARDs) and DEX on IL-1 beta and IL-6 production by IL-1 beta stimulated synovial culture cells].
作者信息
Koda M, Yoshino S, Nakamura H, Asano G
机构信息
Department of Joint Diseases, Nippon Medical School First Hospital, Tokyo, Japan.
出版信息
Nihon Ika Daigaku Zasshi. 1996 Oct;63(5):419-23. doi: 10.1272/jnms1923.63.419.
UNLABELLED
To investigate the effects of disease modifying antirheumatic drugs (DMARDs) and DEX on production of IL-1 beta, IL-6 and TNF-alpha, synovial cells were observed after IL-1 beta administration in vitro.
MATERIALS AND METHODS
Synovial tissue was obtained aseptically from 8 rheumatoid arthritis patients during joint surgery. The dissected tissue was treated with collagenase and adherent cells were passaged before using as samples. They were stimulated with IL-1 beta (1 ng/ml) and cultured with DMARDs and DEX in serum-free media. After 24 hours' incubation, the production of IL-1 beta, IL-6 and TNF-alpha in the supernatants was measured.
RESULTS
DEX inhibited the production of IL-6. GST inhibited the production of IL-1 beta and IL-6.
CONCLUSION
DEX and GST may modulate the disease activity by inhibiting the cytokine production from synovial cells.
未标记
为研究改善病情抗风湿药（DMARDs）和地塞米松（DEX）对白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）产生的影响，在体外给予IL-1β后观察滑膜细胞。
材料与方法
在关节手术期间从8例类风湿性关节炎患者无菌获取滑膜组织。将解剖后的组织用胶原酶处理，贴壁细胞传代后用作样本。用IL-1β（1纳克/毫升）刺激它们，并在无血清培养基中与DMARDs和DEX一起培养。孵育24小时后，测量上清液中IL-1β、IL-6和TNF-α的产生。
结果
DEX抑制IL-6的产生。谷胱甘肽硫转移酶（GST）抑制IL-1β和IL-6的产生。
结论
DEX和GST可能通过抑制滑膜细胞产生细胞因子来调节疾病活动。
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