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目的:基于观察肿瘤骨转移大鼠转移灶周围骨组织TRPA1和TRPM8表达变化以及冷刺激缩足阈值改变,阐释骨癌痛虚寒型冷痛病机。方法:健康4月龄SD雄性大鼠45只,体质量440~470 g,随机分成模型组(仅造模,无药物干预)、模型-通道阻滞剂干预组(造模2周后应用TRPA1、TRPM8拮抗剂干预的大鼠);空白组(正常健康大鼠,无药物干预)。分别于造模前1周、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;并在造模后8周处死大鼠,取转移灶周围骨组织样本,观察组织病理切片形态,并检测TRPA1、TRPM8基因量及蛋白表达水平。结果:造模后2周,模型组大鼠出现明显的冷刺激痛敏,至造模后8周其冷刺激痛阈仍维持较低水平,应用TRPA1、TRPM8通道阻断剂后,骨癌痛大鼠的冷刺激痛阈能显著恢复至接近正常水平。结论:TRPA1、TRPM8通道蛋白表达的上调参与构建了骨癌痛大鼠虚寒型冷痛的病机基础。
OBJECTIVE: To interpret the changes of TRPA1 and TRPM8 in the bone around the tumor metastasis and the change of the threshold of cold stimulus to explain the cold pain syndrome of painful cold syndrome in bone cancer. Methods: 45 healthy male SD rats aged 4 months were randomly divided into model group (model only, no drug intervention) and model-channel blocker intervention group (model group) , TRPM8 antagonist intervention rats); blank group (normal healthy rats, no drug intervention). One week before model making, 2, 4, 6, 8 weeks after model making, 5 rats were randomly selected from 3 groups to measure the incubation period of cold contraction feet. Rats were sacrificed 8 weeks after model establishment, Samples of bone tissue around the foci were observed histopathological sections and TRPA1, TRPM8 gene quantity and protein expression levels. Results: At 2 weeks after model establishment, the rats in the model group showed obvious pain sensation of cold stimulation, and the pain threshold of cold stimulation remained low until 8 weeks after model establishment. After applying TRPA1 and TRPM8 channel blockers, Cold stimulation of pain threshold in rats can be significantly restored to near normal levels. Conclusion: Upregulation of TRPA1 and TRPM8 channel proteins is involved in the construction of the pathogenesis of cold pain in rats with bone cancer pain.