Henderson B, Pettipher E R, Murphy G
Department of Pharmacology, Wellcome Research Laboratories, Kent, United Kingdom.
Arthritis Rheum. 1990 Feb;33(2):241-6. doi: 10.1002/art.1780330213.
Chronic monarticular arthritis can be induced in ovalbumin-sensitized rabbits by intraarticular injection of ovalbumin (antigen-induced arthritis) or in naive rabbits by injecting hyaluronic acid mixed with the polycation poly-D-lysine (polycation-induced arthritis). Both models show some points of similarity, including joint swelling, the presence of inflammatory leukocytes and the inflammatory mediator prostaglandin E2, and the kinetics of cartilage proteoglycan loss. However, the assessment of the capacity of synovial lining and articular cartilage to synthesize and secrete neutral metalloproteinases reveals a difference between these models. We found that articular cartilage from the inflamed joints of rabbits with antigen-induced arthritis did not synthesize neutral metalloproteinases, although the synovial lining did. In contrast, both the synovial lining and the articular cartilage from the inflamed joints of rabbits with polycation-induced arthritis synthesized neutral metalloproteinases. These findings suggest that in inflammatory synovitis, different mechanisms can operate to produce damage to the matrix of articular cartilage.
通过关节内注射卵清蛋白（抗原诱导性关节炎）可在卵清蛋白致敏的兔子中诱发慢性单关节关节炎，或者通过注射与聚阳离子聚-D-赖氨酸混合的透明质酸（聚阳离子诱导性关节炎）在未致敏的兔子中诱发慢性单关节关节炎。两种模型都显示出一些相似之处，包括关节肿胀、炎性白细胞的存在以及炎性介质前列腺素E2，还有软骨蛋白聚糖丢失的动力学。然而，对滑膜衬里和关节软骨合成与分泌中性金属蛋白酶能力的评估揭示了这些模型之间的差异。我们发现，抗原诱导性关节炎兔子炎症关节的关节软骨不合成中性金属蛋白酶，尽管滑膜衬里会合成。相比之下，聚阳离子诱导性关节炎兔子炎症关节的滑膜衬里和关节软骨都合成中性金属蛋白酶。这些发现表明，在炎性滑膜炎中，不同的机制可导致关节软骨基质受损。
