中文摘要：

[目的]观察电针对完全弗氏佐剂（Complete Freund＇s adjuvant,CFA）诱导的慢性炎性痛大鼠痛情绪行为的干预作用及其对前扣带皮层（Anterior Cingulate Cortex,ACC）内蛋白激酶Cζ（Protein Kinase C zeta,PKCζ）的调控。[方法]将健康雄性SD大鼠完全随机分为空白对照组（N组）、模型对照组（CFA组）和电针治疗组（EA组）,每组8只。建立慢性炎性痛模型,选取双侧＂足三里＂、＂昆仑＂穴进行电针治疗,每日1次,连续3天,检测大鼠造模前及造模后ld、3d、7d、14d、21d、28d患侧足跖缩足阈（paw withdrawal thresholds,PWTs）,观察大鼠痛觉超敏反应。用旷场试验和高架O迷宫实验分别观察大鼠造模后29d和30d情绪变化,免疫印迹法检测大鼠双侧ACC内PKCζ和磷酸化PKCζ（p-PKCζ）蛋白表达。[结果]造模前,各组大鼠PWTs差异无统计学意义（P〉0.05）;造模后CFA组大鼠各时点PWTs均明显下降,差异有统计学意义（P〈0.01）,EA组大鼠造模后28d PWTs明显高于CFA组,差异有统计学意义（P〈0.05）。CFA组大鼠造模后29d中央区运动距离、进入中央区次数和中央区停留时间明显减少（P〈0.05）,EA组大鼠中央区运动距离、进入中央区次数和中央区停留时间显著增加,差异有统计学意义（P〈0.01）,CFA组造模后30d进入开放臂次数明显减少,差异有统计学意义（P〈0.05）。CFA组患侧PKCζ和p-PKCζ蛋白表达均明显上升,差异有统计学意义（P〈0.05）,EA组大鼠双侧PKCζ和pPKCζ蛋白表达无统计学意义（P〉0.05）。[结论]电针可减轻慢性炎性痛大鼠痛感觉和痛情绪行为,但其机制可能不是通过调节ACC中PKCζ表达来实现。

英文摘要：

[Objective] To observe the intervention effect of electroacupuncture（EA） on pain-relative behaviour and it ＇s regulation of Protein Kinase C zeta（PKCζ） in anterior cingulated cortex（ACC） of rats with CFA chronic inflammatory pain. [Methods] Healthy male Sprague-Dawley（SD） rats were randomly divided into three groups： N group, CFA group and EA group, each group contained 8 rats. Rat chronic inflammatory pain model was established by CFA. EA was administered at bilateral points Zusanli（ST36） and Kunlun（BL60） once every day for consecutive 3 days. Paw withdraw thresholds（PWTs） were measured before CFA injection, as well as at 1, 3, 7, 14, 21, 28 days after CFA injection. The open-field test and elevated-zero-maze test were respectively observed the emotional behavior of rats on 29 d, 30 d. The protein expression of PKCζ and p-PKCζ in bilateral ACC was detected by western blot. [Result] There were no statistical significant differences of PWTs among the three groups before injecting CFA（ P0.05）. PWTs in CFA group was significantly lower at every time after CFA injection（P0.01）. PWTs in EA group were significantly higher on 28d（P0.05）. The distances in central zone, entries in central zone and times in central zone in CFA group on 29 d were significantly lower than N group, with differences of statistical meaning（ P 0.05）. The distances in central zone,entries in central zone and times in central zone in EA group were significantly higher（P0.01）. Entries in open arms in CFA group on 30 d were significantly lower（P0.05）. The protein expression of PKCζ and p-PKCζ in ipsilateral ACC of CFA rats on 30 d were increased with obvious significance（P〈0.05）. The expression of PKCζ and p-PKCζ in contralateral ACC of EA rats didn＇t have statistical significance（P〉0.05）. [Conclusion] EA could relieve chronic inflammatory pain and pain-relative behaviour induced by CFA, but its mechanism might not be through adjusting the protein expression of PKC ζ in AC