ROLE OF TNFα, IN RELATION TO IL-1 AND IL-6 IN THE PROTEOGLYCAN TURNOVER OF HUMAN ARTICULAR CARTILAGE
ROLE OF TNFα, IN RELATION TO IL-1 AND IL-6 IN THE PROTEOGLYCAN TURNOVER OF HUMAN ARTICULAR CARTILAGE
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TNFα 与 IL-1 和 IL-6 在人类关节软骨蛋白聚糖周转中的作用
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
O. Huber
中科院分区：
文献类型：
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作者：
B. Wilbrink;J. J. Nietfeld;W. Otter;J. L. A. M. Roy;J. Bijlsma;O. Huber
在年轻人和老年人的关节软骨移植中，肿瘤坏死因子α诱导浓度依赖的、可逆的蛋白多糖(PG)合成抑制。青年软骨对肿瘤坏死因子α的敏感性高于老年软骨：当浓度分别为5U/ml和30U/ml时，青年软骨PG合成抑制达50%，而当浓度为10(3)U/ml时，青年软骨PG合成受阻，老年软骨PG合成抑制80%。这些PG合成的抑制水平导致培养8天后外植体耗尽25%的PG。对软骨PG的释放无促进作用。肿瘤坏死因子α在年轻或老年软骨中未诱导可检测到的IL-1量(小于0.01U)，但确实诱导了IL-6的产生。青年软骨IL-6诱导量高于老年软骨，但无明显的剂量依赖性。IL-1和IL-6抗体均不影响肿瘤坏死因子α对PG合成的抑制作用。肿瘤坏死因子α和IL-1联合作用对PG合成有相加的抑制作用，但与IL-6的诱导作用无关。肿瘤坏死因子α的活性大约是IL-1的100倍。
In both young and old human articular cartilage explants, TNF alpha induced a concentration-dependent, reversible suppression of the proteoglycan (PG) synthesis. Young cartilage was more sensitive to TNF alpha than old cartilage: 50% suppression of PG synthesis was reached at a TNF alpha concentration of 5 U/ml for young and 30 U/ml for old cartilage, whereas at 10(3) U/ml the PG synthesis of young cartilage was blocked and that of old cartilage suppressed by 80%. These inhibition levels of PG synthesis resulted in 25% PG depletion of the explants after 8 days of culture. The release of cartilage PG was not enhanced. TNF alpha induced no detectable amounts of IL-1 (less than 0.01 U) in young or old cartilage but did induce IL-6 production. The induced amounts of IL-6 were higher in young than in old cartilage but no dose-dependency was evident. Antibodies to neither IL-1 nor IL-6 had any influence on the TNF alpha-induced suppression of PG synthesis. The combination of TNF alpha and IL-1 led to an additive inhibition of PG synthesis which had no relationship to induced IL-6. TNF alpha was about 100-fold less active than IL-1