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为了探讨脊髓谷氨酸转运体1(GLT-1)的表达量和活性状态与吗啡耐受和神经源性痛的关系,利用大鼠坐骨神经慢性压迫损伤(CCI)模型,以机械性缩足痛阈值(MWT)为评估指标,谷氨酸转运体激动剂β内酰胺类抗生素头孢曲松钠为工具药,观察对大鼠机械痛敏和吗啡耐受的影响;以实时定量PCR及Western blotting考察脊髓GLT-1表达水平的变化。结果表明,CCI大鼠在术后1周与对照组相比MWT值下降约80%;CCI大鼠单独使用吗啡产生快速耐受,给药第3天与CCI模型对照组大鼠比较MWT值已无明显差异,脊髓GLT-1表达也明显下调;单独使用头孢曲松钠对痛敏有改善作用,脊髓GLT-1表达明显上调;吗啡伴随头孢曲松钠给药组耐受速度明显减慢,给药6天后MWT值仍保持在较高水平,与CCI吗啡耐受组比较有显著性差异,GLT-1表达明显上调。因此,脊髓GLT-1活性变化与神经源性痛及吗啡耐受的形成密切相关,促进GLT-1功能可显著延缓吗啡耐受与痛敏形成。
To investigate the relationship between glutamate transporter 1 (GLT-1) expression and activity status with morphine tolerance and neurogenic pain, a rat model of chronic constriction injury (CCI) Threshold (MWT) was used as the evaluation index. The effect of glutamic acid transporter agonist β-lactam antibiotic ceftriaxone sodium on mechanical pain and morphine tolerance was observed. The spinal cord was detected by real-time quantitative PCR and Western blotting GLT-1 expression level changes. The results showed that the MWT value of CCI rats decreased about 80% compared with that of the control one week after the operation. The fast tolerance of morphine to CCI rats alone was achieved. Compared with CCI model control rats on the third day, the MWT value was No significant difference in the expression of GLT-1 in the spinal cord was also significantly reduced; the use of ceftriaxone sodium alone improved the role of pain, spinal cord GLT-1 expression was significantly increased; morphine with ceftriaxone sodium administration group was significantly slower, After 6 days of administration, the MWT value remained at a high level, which was significantly different from CCI morphine tolerant group, and the GLT-1 expression was significantly increased. Therefore, the change of GLT-1 activity in spinal cord is closely related to the formation of neurogenic pain and morphine tolerance. Promoting the function of GLT-1 can significantly delay the morphine tolerance and the formation of hyperalgesia.