Evaluation of the suppressive actions of glucosamine on the interleukin-1β-mediated activation of synoviocytes
Evaluation of the suppressive actions of glucosamine on the interleukin-1β-mediated activation of synoviocytes
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DOI：
10.1007/s00011-007-7020-7
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发表时间：
2007-10-01
影响因子：
6.7
通讯作者：
Nagaoka, I.
中科院分区：
文献类型：
--
作者：
Hua, J.;Sakamoto, K.;Nagaoka, I.
目的：最近，我们发现给药葡萄糖胺佐剂关节炎，类风湿关节炎模型，抑制关节炎的进展。为了阐明其抗炎机制，我们在体外研究了葡萄糖胺对滑膜细胞活化的作用。材料和方法：用白细胞介素(IL)-1 β在0.01-1 mM氨基葡萄糖的存在下刺激人滑膜组织中的滑膜细胞。ELISA法检测IL-8、前列腺素（PG） E含量，Griess法检测一氧化氮含量。RT-PCR检测IL-8 mRNA表达。此外，葡萄糖胺对p38丝裂原活化蛋白激酶（MAPK）磷酸化的影响以及[I-125] IL-1 β与其受体结合的影响通过人滑膜细胞系（CS-ABI-479）进行了研究。结果：氨基葡萄糖显著抑制IL-1 β诱导的IL-8产生及其mRNA表达（p < 0.05），且氨基葡萄糖（1 mM）抑制IL-1 β诱导的一氧化氮和PGE(2)产生（p < 0.05）。此外，葡萄糖胺抑制IL-1 β诱导的p38 MAPK磷酸化（p < 0.05）和IL-1 β与其受体的结合（p < 0.05）。结论：这些观察结果表明，葡萄糖胺可以抑制IL-1 β介导的滑膜细胞活化（如IL-8-、一氧化氮-和PGE(2)-的产生，以及p38 MAPK的磷酸化），从而可能在关节炎中表现出抗炎作用。
Objective: Recently, we found that administration of glucosamine to adjuvant arthritis, a model for rheumatoid arthritis, suppressed the progression of arthritis in rats. To clarify its anti-inflammatory mechanism, we evaluated the actions of glucosamine on the activation of synoviocytes in vitro.Materials and methods: Synoviocytes isolated from human synovial tissues were stimulated with interleukin (IL)-1 beta in the presence of 0.01-1 mM glucosamine. IL-8 and prostaglandin (PG) E, were measured by ELISA, and nitric oxide was quantitated by Griess assay. IL-8 mRNA was detected by RT-PCR. Furthermore, the effect of glucosamine on the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and the binding of [I-125] IL-1 beta to its receptors were examined using a primary human synovial cell line (CS-ABI-479).Results: Glucosamine significantly suppressed the IL-1 beta-induced IL-8 production as well as its mRNA expression (p < 0.05) at 1 mM. Furthermore, glucosamine (1 mM) inhibited the IL-1 beta-induced nitric oxide and PGE(2) production (p < 0.05). Moreover, glucosamine suppressed the IL-1 beta-induced phosphorylation of p38 MAPK (p < 0.05 at >0.1 mM) and the IL-1 beta-binding to its receptors (p < 0.05 at 1 mM).Conclusions: These observations suggest that glucosamine can suppress the IL-1 beta-mediated activation of synoviocytes (such as IL-8-, nitric oxide- and PGE(2)-production, and phosphorylation of p38 MAPK), thereby possibly exhibiting anti-inflammatory actions in arthritis.