骨关节炎关节滑液中IL-18与PGE_2含量的测定及意义

Concentration of IL-18 and PGE_2 in synovial fluid in patients with osteoarthritis and its significance

目的:检测膝关节滑液(synovialfluid,SF)中细胞因子白介素-18(interleukin-18,IL-18)和炎症介质前列腺素E2(prostaglandinE2,PGE2)含量,探讨IL-18和PGE2在骨关节炎(osteoarthritis,OA)发病机制中的作用。方法:提取54例膝OA患者(OA组)的关节滑液,9例对照组(正常组)膝关节液,用ELISA酶联免疫吸附法和酶联免疫竞争法分别检测IL-18和PGE2含量,并对IL-18和PGE2两指标作线性相关与回归分析。结果:OA组膝关节滑液中IL-18和PGE2含量与正常组比较,有增高的趋势,差异有统计学意义(P<0.01)。对照组IL-18浓度值为(28.768±13.575)×10-9ng/L,OA组IL-18浓度值为(72.303±40.130)×10-9ng/L(P<0.01)。对照组PGE2浓度值为(24.697±7.814)×10-9ng/L,OA组PGE2浓度值为(42.302±23.818)×10-9ng/L(P<0.01)。分析表明IL-18与PGE2有较强正相关关系(对照组r=0.76,P<0.001;OA组r=0.94,P<0.001)。结论:本研究表明OA组关节滑液中IL-18与PGE2的含量明显高于对照组,说明IL-18与PGE2可能参与了骨关节炎的发病机制。IL-18的增高可能引起PGE2含量的增高,从而在OA的发病机制中发挥重要作用。

Objective To detect the concentrations of interleukin-18 （IL-18 ） and prostaglandin E2 （ PGE2 ） in synovial fluid （ SF ） , and to determine the role of IL- 18 and PGE2 in osteoarthrifts （OA） pathogenesis. Methods IL-18 and PGE2 were measured concurrently in synovial fluid samples from 54 patients with knee OA （ OA group ） and from 9 controls （ control group ）. Quantitative determination of IL- 18 was performed by enzyme-linked immunosorbent assay （ ELISA ）. PGE2 was examined by inhibitory enzyme-linked immunosorbent assay. A linear regression between IL-18 and PGE2 was anaylsed. Results The concentrations of IL-18 and PGE2 in SF from the OA group were significantly higher than those from the control group （ P 〈 0.01 ）. The average value of IL- 18 in the control group was （28. 768 ± 13. 575） × 10^-9 ng/L, and （72. 303 ±40. 130） × 10^-9 ng/L in the OA group （ P 〈 0.01 ） ; the average value of PGE2 in the control group was （ 24. 697 ± 7.814） ×10^-9 ng/L, and （42.302±23. 818） × 10^-9 ng/L in the OA group （P 〈0. 01）. IL-18 was related with PGE2 in a linear curve fashion （the control group： r = 0.76, P 〈 0. 001 ;the OA group： r = 0. 94, P 〈 0. 001 ）. Conclusion IL-18 and PGE2 are significantly higher in the OA group than those in the control group, and they might take part in the cartilage degradation in OA pathogenesis. The increase of IL-18 might induce the increase of PGE2 , and that might play an important role in OA pathogenesis.