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基于thermoTRP介导冷痛敏机制对膝骨关节炎虚寒冷痛的研究

邢润麟 王培民 茆军 张农山 赵凌睿 李晓辰

邢润麟, 王培民, 茆军, 张农山, 赵凌睿, 李晓辰. 基于thermoTRP介导冷痛敏机制对膝骨关节炎虚寒冷痛的研究[J]. 南京中医药大学学报, 2016, 32(4): 347-351.
引用本文: 邢润麟, 王培民, 茆军, 张农山, 赵凌睿, 李晓辰. 基于thermoTRP介导冷痛敏机制对膝骨关节炎虚寒冷痛的研究[J]. 南京中医药大学学报, 2016, 32(4): 347-351.
XING Runlin, WANG Peimin, MAO Jun, ZHANG Nongshan, ZHAO Lingrui, LI Xiaochen. Mechanism of thermoTRP Participating in Cold Hyperalgesia of Rat with Experimental Knee Osteoarthritis[J]. Journal of Nanjing University of traditional Chinese Medicine, 2016, 32(4): 347-351.
Citation: XING Runlin, WANG Peimin, MAO Jun, ZHANG Nongshan, ZHAO Lingrui, LI Xiaochen. Mechanism of thermoTRP Participating in Cold Hyperalgesia of Rat with Experimental Knee Osteoarthritis[J]. Journal of Nanjing University of traditional Chinese Medicine, 2016, 32(4): 347-351.

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: 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。

     

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  • 刊出日期:  2016-07-10

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