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房春燕,王 燕,王亚南,孟 蒂,张广学,李 宁.伏核内勿动蛋白A和降钙素基因相关肽1受体在炎性痛大鼠痛觉调制过程中的角色[J].中国康复医学杂志,2013,28(1):9~12
伏核内勿动蛋白A和降钙素基因相关肽1受体在炎性痛大鼠痛觉调制过程中的角色    点此下载全文
房春燕  王 燕  王亚南  孟 蒂  张广学  李 宁
潍坊医学院应用药理学实验室,261053
基金项目:山东省自然科学基金资助项目(ZR2009CL049)
DOI:
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摘要:
      摘要 目的:探讨大鼠伏核内勿动蛋白A(Nogo-A)和降钙素基因相关肽1(CGRP1)受体在痛觉调制过程中的作用。 方法:健康雄性SD大鼠随机分为4组:空白对照组,伏核内注射生理盐水1μl;炎性痛模型对照组、吗啡组和纳洛酮组。福尔马林致炎成功后,分别向其伏核内注射生理盐水、吗啡、纳洛酮各1μl。采用Western blot法,观察各组大鼠伏核内Nogo-A和CGRP1受体蛋白表达的变化,分析炎性痛、吗啡、纳洛酮对大鼠伏核内Nogo-A和CGRP1受体蛋白表达的影响。 结果:正常大鼠伏核内有Nogo-A和CGRP1受体蛋白表达;福尔马林致炎后Nogo-A的蛋白表达量降低(P<0.05),而CGRP1表达升高(P<0.05);与炎性痛模型对照组比较,吗啡组大鼠伏核内Nogo-A的蛋白表达量增高(P<0.05),CGRP1降低(P<0.05),而纳洛酮组Nogo-A降低(P<0.05),CGRP1增高(P<0.05)。 结论:Nogo-A和CGRP参与了炎症致痛敏大鼠伏核内的痛觉调制过程,且二者之间存在反向调节关系,内源性阿片系统可能参与并影响了该过程。
关键词:勿动蛋白-A  降钙素基因相关肽受体  吗啡  伏核  痛觉调制
Role of neurite outgrowth inhibitor-A and calcitonin gene related peptide 1 receptor in pain modulation in nucleus accumbens of rats with inflammatory pain    Download Fulltext
Pharmacology Laboratory of Weifang Medical College, 261053
Fund Project:
Abstract:
      Abstract Objective: To investigate the role of neurite outgrowth inhibitor-A(Nogo-A) and calcitonin gene related peptide 1(CGRP1) receptor in pain modulation in nucleus accumbens of rats. Method: Healthy male SD rats were randomly divided into four groups: blank control group (saline was injected to the nucleus accumbens for 1μl); inflammatory pain model control group (formalin was injected to rat's hindpaw to induce inflammatory pain); morphine group and naloxone group (after inflammatory pain models were prepared, morphine and naloxone were injected to nucleus accumbens for 1μl respectively). The Western blot technique was used for Nogo-A and CGRP1 receptor protein recording. The influence of inflammatory pain, morphine and naloxone on Nogo-A and CGRP1 receptor protein expression in nucleus accumbens were analyzed. Result: Nogo-A and CGRP1 receptor proteins expressed in nucleus accumbens of normal rats; the expression of Nogo-A protein decreased significantly(P<0.05)and CGRP1 receptor protein increased significantly(P<0.05)after formalin-induced inflammation. Compared with inflammatory pain model control group, the expression of Nogo-A protein increased significantly(P<0.05)and CGRP1 receptor protein decreased significantly(P<0.05)in morphine group; the expression of Nogo-A protein decreased significantly(P<0.05)and CGRP1 receptor protein increased significantly(P<0.05) in naloxone group. Conclusion: Nogo-A and CGRP were both involved in pain modulation in nucleus accumbens of inflammatory pain rats, and the relationship between Nogo-A and CGRP was negative regulation. Endogenous opioid systems may be influence the role of Nogo-A and CGRP in pain modulation.
Keywords:neurite outgrowth inhibitor-A  calcitonin gene related peptide receptor  morphine  nucleus accumbens  pain modulation
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