Department of Anaesthesiology, Pain and Palliative Medicine, Radboud University Nijmegen Medical Centre, Geert Grootplein zuid 10, Nijmegen, The Netherlands.
Eur J Pharmacol. 2010 Sep 1;641(2-3):108-13. doi: 10.1016/j.ejphar.2010.05.022. Epub 2010 Jun 9.
A rat model of osteoarthritis was used to investigate the effect of pre-treatment with capsaicin on the symptoms of osteoarthritis induced by the injection of monosodium iodoacetate. This model mimics both histopathology and symptoms associated of human osteoarthritis. Injection of monosodium iodoacetate, an inhibitor of glycolysis, into the femorotibial joints of rodents promotes loss of articular trabecular bone and invokes pain symptoms similar to those noted in human osteoarthritis. Twenty rats were divided in two groups either receiving placebo or monosodium iodoacetate. Each group was subdivided in two groups either receiving pre-treatment with capsaicin two weeks before monosodium iodoacetate injection or not, resulting in four groups of five rats each. The impact of a single intra-articular administration of capsaicin (0.5%) on the generation of evoked mechanical pain (hind limb weight bearing, automated von Frey monofilament and RotaRod tests) and bone lesions (micro-CT scan radiographic analyses of bone structure) following monosodium iodoacetate-induced osteoarthritis in rats was determined. Evoked mechanical pain as monitored over a period of 4 weeks after monosodium iodoacetate injection was abolished in capsaicin pre-treated animals and pain values are comparable to those of capsaicin controls. Chronic joint pathological changes such as bone erosion and trabecular damage were significantly reduced by pre-treatment with a single administration of capsaicin. Decrease of bone volume was considerably ameliorated and trabecular connectivity was substantially better in capsaicin pre-treated animals. Capsaicin, an agonist activator of the vanilloid nociceptors (TRPV1), appears to be effective in protecting bone from arthritic damage. The present results support the hypothesis that capsaicin-sensitive sensory neurons contribute to bone lesions in the monosodium iodoacetate-induced osteoarthritis rat model.
一种骨关节炎的大鼠模型被用于研究辣椒素预处理对注射单碘乙酸盐引起的骨关节炎症状的影响。该模型模拟了人类骨关节炎的组织病理学和症状。向啮齿动物的股胫关节注射单碘乙酸盐，一种糖酵解抑制剂，可促进关节小梁骨的丧失，并引发类似于人类骨关节炎的疼痛症状。20 只大鼠被分为两组，一组接受安慰剂，另一组接受单碘乙酸盐注射。每组再分为两组，一组在注射单碘乙酸盐前两周接受辣椒素预处理，另一组不接受，结果分为四组，每组 5 只大鼠。确定单次关节内给予辣椒素（0.5%）对单碘乙酸盐诱导的大鼠骨关节炎后诱发机械性疼痛（后肢负重、自动冯弗雷单丝和旋转棒试验）和骨病变（骨结构的微 CT 扫描放射学分析）的影响。在注射单碘乙酸盐后 4 周的时间内监测到的诱发机械性疼痛在辣椒素预处理的动物中被消除，并且疼痛值与辣椒素对照动物相当。单次给予辣椒素预处理可显著减轻慢性关节病理变化，如骨侵蚀和小梁破坏。骨量减少明显改善，并且在辣椒素预处理的动物中，小梁连接性明显更好。辣椒素是香草素感受器（TRPV1）的激动剂激活剂，似乎能有效保护骨骼免受关节炎损伤。这些结果支持了这样的假设，即辣椒素敏感的感觉神经元有助于单碘乙酸盐诱导的骨关节炎大鼠模型中的骨病变。
