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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Effect of iNOS inhibitor S-methylisothiourea in monosodium iodoacetate-induced osteoathritic pain: Implication for osteoarthritis therapy
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Effect of iNOS inhibitor S-methylisothiourea in monosodium iodoacetate-induced osteoathritic pain: Implication for osteoarthritis therapy

机译：iNOS抑制剂S-甲基异硫脲在碘乙酸单钠诱发的骨关节炎疼痛中的作用：对骨关节炎治疗的意义

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摘要

Much information is available on the role of nitric oxide (NO) in osteoarthritis (OA). However, its role has not been studied in the monosodium iodoacetate (MIA)-induced model of osteoarthritic pain. The present study was undertaken in rats to investigate the effect of iNOS inhibitor S-methylisothiourea (SMT) in MIA-induced osteoathritic pain and disease progression in rats. Osteoarthritis was produced by single intra-articular injection of the MIA in the right knee joint on day 0. Treatment groups were orally gavazed with different doses of SMT (10, 30 and 100 mg/kg) and etoricoxib (10 mg/kg) daily for 21 days. On days 0, 3, 7, 14 and 21, pain was measured and histopathology of right knee joint was done on day 21. SMT produced analgesia in a dose-dependent manner as shown by mechanical, heat hyperalgesia, knee vocalization, knee squeeze test, and spontaneous motor activity test. SMT reduced NO production in synovial fluid. Histopathological findings indicated that SMT reduced disease progression as evident from complete cartilage formation in rats treated with SMT at 30 mg/kg. In conclusion, the results indicate that SMT attenuates the MIA-induced pain and histopathological changes in the knee joint. The antinociceptive and antiarthritic effects of SMT were mediated by inhibiting cartilage damage and suppression of NO in synovial fluid. It is suggested that SMT has potential as a therapeutic modality in the treatment of osteoarthritis. ? 2013 Elsevier Inc.
机译：关于一氧化氮（NO）在骨关节炎（OA）中的作用，可以获得很多信息。但是，它的作用尚未在碘乙酸单钠（MIA）诱导的骨关节炎疼痛模型中进行研究。本研究是在大鼠中进行的，以研究iNOS抑制剂S-甲基异硫脲（SMT）在MIA诱导的大鼠骨关节炎疼痛和疾病进展中的作用。骨关节炎是在第0天通过单次关节内右膝关节内MIA注射产生的。每天给治疗组口服不同剂量的SMT（10、30和100 mg / kg）和依托考昔（10 mg / kg）持续21天。在第0、3、7、14和21天测量疼痛，并在第21天进行右膝关节的组织病理学检查。SMT以剂量依赖的方式产生镇痛作用，如机械，热痛觉过敏，膝盖发声，膝盖挤压试验所示。 ，并进行自发运动活动测试。 SMT减少了滑液中的NO生成。组织病理学结果表明，用30 mg / kg SMT处理的大鼠完全软骨形成可明显证明SMT降低了疾病进展。总之，结果表明，SMT减轻了MIA引起的膝关节疼痛和组织病理学变化。 SMT的抗伤害性和抗关节炎作用是通过抑制软骨损伤和抑制滑液中的NO介导的。提示SMT在治疗骨关节炎方面具有潜力。 ？ 2013爱思唯尔公司

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