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首页> 外文期刊>Osteoarthritis and cartilage >Joint fluid antioxidants are decreased in osteoarthritic joints compared to joints with macroscopically intact cartilage and subacute injury.
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Joint fluid antioxidants are decreased in osteoarthritic joints compared to joints with macroscopically intact cartilage and subacute injury.

机译：与具有宏观完整软骨和亚急性损伤的关节相比，骨关节炎关节中的关节液抗氧化剂减少。

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OBJECTIVE: Excess reactive oxygen species and oxidative damage have been associated with the pathogenesis of osteoarthritis (OA). Extracellular superoxide dismutase (EC-SOD or SOD3) scavenges superoxide is the major catalytic antioxidant in joint fluid and is decreased in OA cartilage. We studied human joint fluid samples to test whether there is an association between OA and EC-SOD or other low molecular antioxidants in the joint fluid. METHODS: Joint fluid samples were obtained from 28 subjects with severe OA undergoing arthrocentesis or knee joint replacement and compared to joint fluid from 12 subjects undergoing knee arthroscopy for chronic knee pain, meniscal tears or anterior cruciate ligament reconstruction. EC-SOD protein was assayed by enzyme-linked immunosorbent assay (ELISA). Ascorbate and urate were measured with high performance liquid chromatography (HPLC) and total nitrates by the Greiss reaction. Glutathione (GSH) and oxidized glutathione were measured using a colorimetric method. Interleukin-6 (IL-6) and transforming growth factor-beta (TGF-beta) were both measured with ELISA. RESULTS: Human joint fluid contains significant amounts of the extracellular, catalytic antioxidant EC-SOD. Joint fluid from OA subjects is characterized by significantly decreased EC-SOD levels and significant decreases in GSH, and ascorbate compared to the reference group of knee joints with pain or subacute injury but macroscopically intact cartilage. GSH and ascorbate show only an age effect with no effect from disease state on regression modeling. Urate is present in joint fluid but does not show a significant difference between groups. IL-6 and TGF-beta both show non-significant trends to increases in the arthritic subjects. There was no correlation of EC-SOD levels with IL-6 as a marker of inflammation in either the comparison group or the OA group. CONCLUSIONS: EC-SOD, the major scavenger of reactive oxygen species (ROS) in extracellular spaces and fluids, is decreased in late stage OA joint fluid compared to fluid from injured/painful joints with intact cartilage. Injured joints may be able to increase or maintain secretion of EC-SOD but it appears that late stage OA joints fail to do so in spite of increased oxidative stress seen in the disease. Associated age related declines in GSH and ascorbate might also contribute to the development of severe OA. The net effect of these changes in joint fluid antioxidants is likely to accelerate the damaging oxidant effects on extracellular matrix stability in cartilage tissue.
机译：目的：过量的活性氧和氧化损伤与骨关节炎（OA）的发病机制有关。细胞外超氧化物歧化酶（EC-SOD或SOD3）清除超氧化物是关节液中的主要催化抗氧化剂，并且在OA软骨中降低。我们研究了人体关节液样本，以测试关节液中OA和EC-SOD或其他低分子抗氧化剂之间是否存在关联。方法：从28例严重OA进行关节穿刺术或膝关节置换术的受试者获得关节液样本，并将其与12例行膝关节镜检查的受试者的关节液进行比较，以评估慢性膝关节疼痛，半月板撕裂或前交叉韧带重建。 EC-SOD蛋白通过酶联免疫吸附测定（ELISA）进行测定。用高效液相色谱（HPLC）测定抗坏血酸盐和尿酸盐，并通过Greiss反应测定总硝酸盐。谷胱甘肽（GSH）和氧化型谷胱甘肽使用比色法测量。白细胞介素6（IL-6）和转化生长因子-β（TGF-β）都通过ELISA进行了测量。结果：人体关节液中含有大量的细胞外催化抗氧化剂EC-SOD。与患有疼痛或亚急性损伤但宏观上完整的软骨的参比组相比，来自OA受试者的关节液的特征在于EC-SOD水平显着降低，GSH和抗坏血酸显着降低。 GSH和抗坏血酸仅显示年龄效应，而疾病状态对回归模型没有影响。尿液存在于关节液中，但两组之间无明显差异。 IL-6和TGF-β均显示出关节炎受试者增加的非显着趋势。在比较组或OA组中，EC-SOD水平与IL-6作为炎症指标均无相关性。结论：EC-SOD是细胞外空间和液体中主要的活性氧清除剂，在晚期OA关节液中，其与软骨受损/关节疼痛的液体相比，其含量降低了。受伤的关节可能能够增加或维持EC-SOD的分泌，但是尽管在该疾病中发现氧化应激增加，但晚期OA关节似乎无法做到这一点。与年龄相关的谷胱甘肽和抗坏血酸下降也可能导致严重的OA。关节液抗氧化剂的这些变化的净作用可能会加速对软骨组织中细胞外基质稳定性的破坏性氧化剂作用。

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