The regulation mechanism of cartilage destruction m osteoarthritis

软骨基质合成与降解的失衡导致关节软骨的破坏。为了了解骨关节炎中软骨破坏的调节机制，我们检测了胰岛素样生长因子（IGF）-I、地塞米松和mdomethacin对软骨组织分解代谢因子白细胞介素（IL）-1β作用的影响。我们进行了软骨细胞的单层或三维培养。在加入IL-1 β和IGF-1、地塞米松或吲哚美辛的情况下，用ELISA法测定培养液中IL-6和基质金属蛋白酶（MMP）-3、-9、-13的浓度。提取细胞总RNA，RT PCR检测细胞中聚集蛋白聚糖、Ⅱ型胶原、IL-6和MMP-3、9、13 mRNA的表达。IL-1 β在蛋白和mRNA水平上增加IL-6和MMPs的表达。IL-1 β的这种作用可被地塞米松和吲哚美辛所抑制，但不被IGF-1所抑制。这些结果表明，不同的机制可能存在于软骨破坏的调节。

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.