基于thermoTRP介导冷痛敏机制对膝骨关节炎虚寒冷痛的研究

Mechanism of thermoTRP Participating in Cold Hyperalgesia of Rat with Experimental Knee Osteoarthritis

    摘要
  • 摘要: 目的 基于膝骨关节炎大鼠冷缩足潜伏期和冷刺激敏感通道蛋白TRPA1和TRPM8在患膝滑膜组织的表达变化，阐述膝骨关节炎虚寒冷痛的形成原理。方法 健康4月龄SD雄性大鼠45只，体质量440~470g，随机分成KOA模型组（仅造模，无药物干预）、拮抗剂干预组（造模2周后应用TRPA1、TRPM8拮抗剂干预的大鼠）；正常组（正常健康大鼠，无药物干预）。分别于造模前3d、造模后2、4、6、8周，在3组中随机选择5只大鼠，测定冷缩足潜伏期；并于造模后第8周测定痛阈值结束后处死大鼠（CO2窒息法），取患膝滑膜、软骨组织样本，观察软骨组织病理切片形态，并检测滑膜组织TRPA1、TRPM8基因量及蛋白表达水平。结果 造模后2周KOA大鼠出现明显的冷刺激痛敏，至造模后4周其冷刺激痛阈仍处于非正常低水平，应用TRPA1、TRPM8抑制剂能够提高KOA大鼠的冷刺激痛阈。结论 TRPA1、TRPM8表达上调参与构建膝骨关节炎冷刺激痛敏，是膝骨关节炎虚寒冷痛形成的重要基础。

     

    Abstract: OBJECTIVE To observe both TRPA1 and TRPM8 expressions in synovial tissues of rats with cold hyperalgesia induced by experimental knee osteoarthritis(KOA). METHODS 45 Sprague Dawley male rats， weight ranging from 440g to 470g were randomly individed into the model group， modelantagonist and normal group. Paw withdrawal latency (PWL) of five rats from each group was determined one week before modeling， 2， 4， 6 and 8 weeks after modeling， respectively. 8 weeks after modeling， the rats were killed and synovial and cartilage tissues from diseased knee were collected， to observe pathological morphology at cartilage tissues and to determine the protein and gene expressions of TRPA1 and TRPM8 at synovial tissues. RESULTS KOA rats showed obvious cold hyperalgesia from two weeks after modeling to the latest followup， 8 weeks after modeling. The abnormally low level of PWL could be increased by TRPA1 and TRPM8 ion channel blocker. CONCLUSION Upregulating expressions of TRPA1 and TRPM8 participate in the occurrence mechanism of KOA cold hyperalgesia.

     

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