The regulation mechanism of cartilage destruction m osteoarthritis

软骨基质合成和降解之间的不平衡导致关节软骨的破坏。为了了解骨关节炎软骨破坏的调节机制，我们研究了胰岛素样生长因子(IGF)- 1、地塞米松和氨基美辛对软骨组织分解代谢因子白介素(IL)-1β的作用。我们进行了软骨细胞的单层或三维培养。用ELISA法检测IL-6和基质金属蛋白酶(MMP)-3、-9、-13的浓度，并测定IL-6和基质金属蛋白酶(MMP)-3、-9、-13的浓度。提取细胞层总RNA， RT - PCR检测聚集蛋白、II型胶原、IL-6和mmp -3,9,13 mRNA的表达。在IL-β存在或不存在的情况下，IGF-I诱导聚集蛋白和胶原II mRNA的表达。il - 1 β增加了IL-6和MMPs在蛋白和mRNA水平上的表达。地塞米松和吲哚美辛可抑制IL-Iβ的这些作用，而IGF-I则不能。这些结果提示软骨破坏的调控可能存在不同的机制。

Imbalances between synthesis and degradation of cartilage matrix lead the destruction of articular cartilage. To know the regulation mechanism of cartilage destruction in osteoarthritis, we have examined the effects of insulin-like growth factor (IGF)-I, dexamethasone, and mdomethacin on the action of interleukin (IL)-1β, which is the catabolic factor for cartilage tissue. We performed monolayer or three dimensional culture of chondrocytes. After adding the IL-I β with or without IGF-I, dexamethasone or indomethacin, the concentration of IL-6 and matrix metalloptroteinase (MMP)-3,-9,-13 in the culture medium was measured by ELISA. Further, total RNA was extracted from the cell layer, and the expression of aggrecan, collagen II, IL-6, and MMP-3,9,13 mRNA was measured by RT PCR.IGF-I induced the expression of aggrecan and collagen II mRNA both in the presence or absence of IL-β. IL-I β increased the expression of IL-6 and MMPs in the protein and mRNA levels. These effects of IL-Iβ was inhibited by dexamethasone and indomethacin but not by IGF-I. These results suggest that different mechanism may exist in the regulation of cartilage destruction.