中文摘要：

目的探讨蛋白激酶C（protein kinase C,PKC）的抑制剂和激动剂对痛觉超敏的影响及其分子机制。方法小鼠后趾皮下注射完全弗氏佐剂（complete Freund＇s adjuvant,CFA）建立炎性疼痛模型;鞘内给予PKC抑制剂白屈菜赤碱（chelerythrine,CHE）或激动剂Phorbol 12-myristate 13-acetate（PMA）前后,测定小鼠缩足阈值;随后立即分离脊髓背角,免疫印迹法检测NMDA（N-methyl-D-aspartate）型谷氨酸受体的突触表达。结果 PKC抑制剂CHE在缓解炎性痛觉超敏的同时,明显翻转脊髓NMDA受体NR2B亚基的突触表达亢进;而正常小鼠鞘内给予PKC激动剂PMA,可模拟CFA的效应,即：诱发痛觉超敏,并特异性增加NR2B亚基的突触含量。结论 PKC通过调节脊髓NMDA受体NR2B亚基的突触表达,参与炎性疼痛的形成。

英文摘要：

Aim To investigate the role of Protein kinase C（PKC）in inflammatory pain and underlying mechanisms.Methods Complete Freund＇s Adjuvant（CFA）was injected into the plantar surface of the hindpaw of mice to induce inflammatory pain.Paw Withdrawal Threshold（PWT）was measured before and after intrathecal administration of PKC blocker Chelerythrine（CHE）or agonist Phorbol 12-myristate 13-acetate（PMA）.Immediately after behavioral test,L4-L5 spinal dorsal horn was removed for inmmunoblotting analysis of the expression of NMDA receptors.Results PKC inhibitor CHE simultaneously reversed the mechanical allodynia and the increase in the synaptic expression of NMDA receptor NR2B subunit in CFA-induced inflamed mice.Direct activation of PKC by intrathecal application of PKC agonist PMA mimicked the effects of CFA by evoking mechanical allodynia and NR2B synaptic accumulation in spinal dorsal horn.Conclusion PKC were involved in the formation of inflammatory pain by regulating synaptic expression of NMDA receptor NR2B subunit.