Flipo R M, Héron F, Huet G, Balduyck M, Degand P, Duquesnoy B, Delcambre B
Clinique Rhumatologique, Hôpital de la Charité, Lille.
Rev Rhum Mal Osteoartic. 1991 Feb;58(2):131-3.
Joint and bone damage in rheumatoid arthritis is thought to be caused primarily by an imbalance between proteolytic proteinases and their specific inhibitors. Matrix destruction can in part result from the activity of lysosomal cystein proteinases such as cathepsin B and L. Cathepsins usually are determined by enzyme immuno-assay. The aim of this study was the direct determination of synovial thiol-proteolytic activity by spectrofluorimetry using a synthetic substrate (Z-Phe-Arg-NMec) and a cystein proteinase specific inhibitor (E64 = L-trans-epoxy-succinyl-leucylamino-(4 guanidino)-butane). 18 rheumatoid synovial fluids were tested compared to 10 osteoarthritic synovial fluids. Thiol-proteolytic activity appeared higher in rheumatoid arthritis compared to osteo-arthrosis (mean value = 1,311 mU/l vs 156 mU/l, p less than 0.01). Synovial thiol-proteolytic activity is well correlated with synovial elastase-alpha1-proteinase-inhibitor complex. The authors found no correlation with synovial polymorphonuclear count (p = 0.38) nor with clinical and biological parameters of disease evolution. The highest values were observed in patient with radiological signs of joint destruction. Synovial thiol-proteolytic activity might represent the potential destructive evolution of rheumatoid arthritis.
类风湿关节炎中的关节和骨骼损伤被认为主要是由蛋白水解蛋白酶与其特异性抑制剂之间的失衡所致。基质破坏部分可归因于溶酶体半胱氨酸蛋白酶（如组织蛋白酶B和L）的活性。组织蛋白酶通常通过酶免疫测定法来测定。本研究的目的是使用合成底物（Z-苯丙氨酸-精氨酸-甲基香豆素酰胺）和半胱氨酸蛋白酶特异性抑制剂（E64 = L-反式环氧琥珀酰基-亮氨酰氨基-（4-胍基）-丁烷），通过荧光分光光度法直接测定滑膜硫醇蛋白水解活性。对18份类风湿性滑液与10份骨关节炎滑液进行了检测。与骨关节炎相比，类风湿关节炎中的硫醇蛋白水解活性似乎更高（平均值 = 1311 mU/l对156 mU/l，p < 0.01）。滑膜硫醇蛋白水解活性与滑膜弹性蛋白酶-α1-蛋白酶抑制剂复合物密切相关。作者发现其与滑膜多形核细胞计数（p = 0.38）以及疾病进展的临床和生物学参数均无相关性。在有关节破坏放射学征象的患者中观察到最高值。滑膜硫醇蛋白水解活性可能代表类风湿关节炎潜在的破坏性进展。
