论文部分内容阅读
目的 :探讨一氧化氮合酶 (nitricoxidesynthase ,NOS)抑制剂在实验性骨关节炎 (osteoarthritis,OA)关节滑液中对前列腺素E2 (prostaglandinE2 ,PGE2 )的调节作用 ,为研制针对NO治疗OA的药物提供理论依据。方法 :采用兔右后腿膝关节伸直位石膏管固定建立实验性OA模型 ,同时建立对照组 ,分别给予NOS抑制剂L 硝基精氨酸甲酯 (L NAME)或环氧化酶 2(COX 2 )抑制剂塞来昔布 ,检测各实验组关节滑液中的NO水平与PGE2 的含量。结果 :L NAME +石膏固定组的NO水平和PGE2 浓度 ,明显比单纯石膏固定组低 ,两者的差异有显著的统计意义 (P <0 .0 1) ,而塞来昔布 +石膏固定组的NO水平 ,与单纯石膏固定组NO水平比较 ,两者的差异没有显著的统计学意义 (P >0 .0 5 )。结论 :实验性OA关节滑液中 ,NOS抑制剂L NAME不仅能有效降低OA关节滑液中NO的水平 ,同时下调PGE2 的浓度 ,而COX 2抑制剂对NO的水平无明显影响
Objective: To investigate the regulatory effect of nitric oxide synthase (NOS) inhibitor on prostaglandin E2 (PGE2) in experimental synovial fluid of osteoarthritis (OA) Drugs provide a theoretical basis. Methods: The model of experimental OA was established by the extension of the right knee of the knee with plaster tube in the right hind leg. At the same time, the control group was given the NOS inhibitor L NAME or cyclooxygenase 2 COX 2) inhibitor celecoxib, the synovial fluid of each experimental group to detect the level of NO and PGE2 content. Results: The levels of NO and PGE2 in the LAME + gypsum group were significantly lower than those in the gypsum group (P <0.01), while the difference between the two groups was statistically significant (P <0.01), while the celecoxib plus gypsum group The level of NO was not significantly different from the level of NO in pure plaster fixation group (P> 0.05). CONCLUSIONS: In experimental OA synovial fluid, NOS inhibitor L NAME can not only effectively reduce the level of NO in synovial fluid of OA, but also decrease the concentration of PGE2, while COX 2 inhibitor has no effect on the level of NO