创伤性关节炎软骨中基质金属蛋白酶13及组织特异性抑制剂1的表达*

背景：关节软骨损伤后继发性退变机制仍不十分清楚。近年研究发现关节软骨细胞外基质合成与降解失衡是造成软骨变性的重要原因之一,其中基质金属蛋白酶可能起决定性的作用。 目的：观察基质金属蛋白酶13及其组织特异性抑制剂1在创伤性关节炎中的表达及与软骨退变的关系。 方法：将新西兰兔分别用骨水泥制作的模具从1.33 kg,46 cm高度和0.43 kg,20 cm高度进行自由落体撞击制备轻型和重型撞击创伤性关节炎兔模型。 结果与结论：苏木精-伊红染色和免疫组织化学染色结果显示,基质金属蛋白酶13和组织特异性抑制剂1在两组均增高(P < 0.05)。组织特异性抑制剂1在重型撞击创伤性关节炎模型兔软骨组织中的分泌明显高于轻型撞击组(P < 0.05)。说明关节软骨在创伤后,基质金属蛋白酶13及组织特异性抑制剂1表达上调,共同作用促进了关节软骨退变,其中组织特异性抑制剂1的过量表达可能是造成关节软骨进一步损害的原因之一。

Expression of matrix metalloproteinase 13 and tissue inhibitor of metalloproteinase 1 in cartilage of traumatic osteoarthritis models

BACKGROUND: The mechanism of articular cartilage degeneration in traumatic osteoarthritis is not yet clear. In recent years, studies found that imbalance of synthesis and degradation of extracellular matrix is one of the important reasons for the cartilage degeneration. Matrix metalloproteinase (MMPs) may plays a decisive role in this process. OBJECTIVE: To investigate the expression of MMPs-13 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in cartilage of traumatic arthritis model, and relationship between MMPs-13, TIMP-1 and cartilage degeneration. METHODS: Healthy adult New Zealand rabbits were used to construct mild and severe traumatic arthritis models which were established with gravity method (1.33 kg, 46 cm height and 0.43 kg, 20 cm height, respectively). RESULTS AND CONCLUSION: Hematoxylin-eosin staining and immunohistochemical staining showed that the expression of both MMP-13 and TIMP-1 were significantly increased in the mild and severe traumatic groups (P < 0.05). Expression of TIMP-1 in the severe traumatic group was higher than that of in the mild traumatic group (P < 0.05). This shows that there is certain increase of MMP-13 and TIMP-1 in post-traumatic osteoarthritis. MMP-13 and TIMP-1 together to promote the degeneration of articular cartilage, and the over-expression of TIMP-1 may be one of the reasons in the further impairment to articular cartilage.