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目的:研究辣椒素受体(transient receptor potential vanilloid type1,TRPV1)和氨基端激酶(c-Jun N-Terminal Kinase,JNK)在树脂毒素(Resiniferatoxin,RTX)致痛模型大鼠中的作用及其与行为学之间的关系。方法:SD大鼠分为Sham组,RTX处理组,RTX处理capsazepine(TRPV1抑制剂)治疗组和RTX处理SP600125(JNK抑制剂)治疗组。每组分别于RTX处理前2 d,处理后5周内每隔3 d进行痛行为学检测。采用Western Blot测定脊髓TRPV1和JNK的表达水平。结果:与Sham组相比,RTX处理1 d后脊髓内TRPV1表达降低同时出现热痛阈升高(P<0.05),10 d后p-JNK表达升高同时出现机械痛阈降低(P<0.05),以上变化都持续超过5周。预先鞘内给予capsazepine可延缓热痛阈升高和上调脊髓TRPV1表达(P<0.05)。机械痛敏形成后给予SP600125可有效缓解病理性痛以及下调脊髓p-JNK的表达(P<0.05)。结论:TRPV1和p-JNK可能与RTX致痛模型大鼠中神经痛的形成相关。
AIM: To investigate the role of TRPV1 and JNK in the rat model of resiniferatoxin (RTX) pain and its relationship with The relationship between behavior. Methods: The SD rats were divided into sham group, RTX group, RTX group, capsazepine (TRPV1 inhibitor) group and RTX group (JNK inhibitor group). The pain behavior test was performed every 3 days in each group within 2 days before RTX treatment and within 5 weeks after the treatment. Western Blot was used to detect the expression of TRPV1 and JNK in the spinal cord. Results: Compared with Sham group, the expression of TRPV1 in spinal cord decreased and the pain threshold increased at 1 d after RTX treatment (P <0.05). After 10 days, the expression of p-JNK increased and mechanical pain threshold decreased (P <0.05 ), The above changes have lasted more than 5 weeks. Preincubation of capsazepine intrathecally delayed the increase of thermal pain threshold and up-regulated TRPV1 expression in the spinal cord (P <0.05). After the formation of mechanical hyperalgesia, administration of SP600125 could effectively relieve pathological pain and down-regulate the expression of p-JNK in the spinal cord (P <0.05). Conclusion: TRPV1 and p-JNK may be related to the formation of neuralgia in rats with RTX-induced pain.