白细胞介素-4对人关节软骨细胞基质金属蛋白酶-3合成的抑制作用。
Suppression of matrix metalloproteinase-3 synthesis by interleukin-4 in human articular chondrocytes.
作者信息
Nemoto O, Yamada H, Kikuchi T, Shinmei M, Obata K, Sato H, Seiki M
机构信息
Department of Orthopaedic Surgery, National Defense Medical College, Saitama, Japan.
出版信息
J Rheumatol. 1997 Sep;24(9):1774-9.
OBJECTIVE
To evaluate the effect of interleukin-4 (IL-4) on IL-1 induced matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1) production by human articular chondrocytes.
METHODS
Monolayer cell culture of chondrocytes was obtained from human articular cartilage from patella within 24 h after death. MMP-3 and TIMP-1 protein levels were determined by ELISA. MMP-3 activity was assayed as caseinase activity. Amounts of MMP-3 and TIMP-1 mRNA were measured by Northern blot analysis.
RESULTS
IL-4 suppressed IL-1 stimulated MMP-3 protein and enzyme activity. Moreover, IL-4 suppressed IL-1 induced MMP-3 mRNA. In contrast, IL-4 did not alter the level of TIMP-1 protein and mRNA.
CONCLUSION
IL-4 may be implicated as a protective mediator of joint destruction seen in inflammatory arthritis.
目的
评估白细胞介素-4（IL-4）对白细胞介素-1（IL-1）诱导人关节软骨细胞产生基质金属蛋白酶-3（MMP-3）和金属蛋白酶组织抑制剂-1（TIMP-1）的影响。
方法
在人死后24小时内从髌骨的关节软骨获取软骨细胞进行单层细胞培养。通过酶联免疫吸附测定法（ELISA）测定MMP-3和TIMP-1蛋白水平。以酪蛋白酶活性测定MMP-3活性。通过Northern印迹分析测量MMP-3和TIMP-1 mRNA的量。
结果
IL-4抑制IL-1刺激的MMP-3蛋白和酶活性。此外，IL-4抑制IL-1诱导的MMP-3 mRNA。相反，IL-4未改变TIMP-1蛋白和mRNA的水平。
结论
IL-4可能作为炎症性关节炎中关节破坏的一种保护性介质。
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