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目的:观察鞘内注射布托啡诺对神经源性疼痛大鼠脊髓NMDAR1、MOR mRNA表达的影响,进而探讨布托啡诺治疗神经源性疼痛的可能机制。方法:健康雄性SD大鼠24只,体重(250±20)g,随机分为3组(n=8),对照组(B组)、生理盐水组(C组)和布托啡诺组(T组)。B组不给予任何干预处理;C组和T组进行鞘内置管并建立大鼠神经病理性疼痛模型(CCI),C组鞘内每天给予10μl生理盐水,T组鞘内每天输注布托啡诺12μg/10μl(生理盐水稀释)。持续7d后,断头处死大鼠,取出脊髓标本,RT-PCR测定NMDAR1和MOR mRNA的表达水平。结果:NMDAR1 mRNA表达,C组与B组相比,NMDAR1 mRNA表达水平显著升高,P<0.01,T组与C组比较表达水平降低,P<0.05。MOR mRNA表达,B组、C组、T组各组间相比,差异无统计学意义。结论:鞘内注射布托啡诺可降低CCI模型引起的大鼠脊髓NMDAR1 mRNA表达水平上调,对MOR mRNA表达水平无影响;CCI模型后12d内MOR mRNA的表达水平恢复正常。
OBJECTIVE: To observe the effects of intrathecal injection of Butorphanol on the expression of NMDAR1 and MOR mRNA in the spinal cord of neuropathic pain rats, and to explore the possible mechanism of butorphanol in the treatment of neuropathic pain. Methods: Twenty-four healthy male SD rats weighing 250 ± 20 g were randomly divided into three groups (n = 8), control group (group B), saline group (group C) and butorphanol group group). Group B received no intrathecal intervention; group C and group T received intrathecal catheterization and establishment of a rat model of neuropathic pain (CCI); Group C received daily intrathecal administration of 10 [mu] l of normal saline; Group T received intrathecal instillation of butorphanol 12 μg / 10 μl (diluted with saline). After 7 days, the rats were sacrificed and their spinal cord specimens were removed. The expression of NMDAR1 and MOR mRNA was detected by RT-PCR. Results: The expression of NMDAR1 mRNA in group C was significantly higher than that in group B (P <0.01). The expression of NMDAR1 mRNA in group C was significantly lower than that in group C (P <0.05). MOR mRNA expression, B group, C group, T group compared to each other, the difference was not statistically significant. Conclusion Intrathecal injection of Butorphanol can reduce the expression of NMDAR1 mRNA induced by CCI in rat spinal cord and has no effect on the expression of MOR mRNA. The expression of MOR mRNA returned to normal within 12 days after CCI.