电针对侧脑室注射孤啡肽实验性RA痛阈和皮肤FOS表达的影响

目的：观察电针对大鼠实验性关节炎痛阈和皮肤c-fos表达的作用及侧脑室注射孤啡肽（OFQ）对电针效应的影响。方法：将福氏完全佐剂（FCA）注入SD大鼠踝关节腔造成类风湿性关节炎的模型。44只SD大鼠随机分为A模型＋侧脑室注射生理盐水（NS）＋电针,n=8],B（模型＋侧脑室注射OFQ＋电针,n＝8）,C（正常对照,n＝8）,D（模型,n＝10）和E（模型＋电针,n＝10）组。大鼠麻醉（戊巴比妥钠30mg/kg,i.p)后,参照Noble方法定位,将OFQ（20μL,50μg/mL）或NS（20μL）注射侧脑室（30min内注完,保留1min）。右侧“太溪”和“足三里”针刺后连接WQ－10C多用途电子穴位测定治疗仪,用疏密波形,频率20／100Hz交替,电压2－4V,波宽0．2－0．6ms,持续20min,电针每天1次,连续5天。痛阈用气压弹簧棒测定后右掌心皮肤加压时动物的缩腿反应,每天1次,共测5天。取大鼠右后足垫部皮肤及皮下组织,采用免疫组织化学ABC法测定RA模型建立后各组c-fos表达。结果与结论：①电针对实验性RA关节痛具有明显的镇痛效应;②电针明显提高实验性RA大鼠痛阈,具有明显的后效应,注射OFQ对抗电针提高实验性RA大鼠痛阈,而且对抗电针的后效应;③电针抑制实验性RA诱导的FOS表达,注射OFQ对抗电针抑制FOS的表达。

Influence of Intraventricular Injection of Orphanin on Electroacupuncture Analgesia and Cutaneous C-fos Expression in Experimental Arthritis Rats

Objective: To observe the effect of electroacupuncture (EA) on pain thresh old and experimental arthritis induced cutaneous c fos expression and the influ ence of intraventricular injection of orphanin (OFQ) on EA analgesia and arthrit is induced c fos expression in rheumatoid arthritis (RA) SD rats. Met hods: 44 SD rats were randomly divided into A RA model + lateral ventri cular injection (LVI) of normal saline 20 μL + EA, n=8, B (model +L VI of OFQ+EA,n=8), C (normal control, n=8), D (RA model , n=10) and E (model+EA, n=10) groups. RA rat model was esta blished by injection of Freund's complete adjuvant into the ankle joint space. A cupoints of "Taixi" (KI 3) and "Zusanli" (ST 36) on the right hindlimb were puncture d and stimulated electrically with WQ 10C Electronic Acupoint Detection and The rapeutic Apparatus by setting the parameters of frequency 2/100 Hz, 2～4 V, wave width 0.2～0.6 ms and stimulating duration 20 min. Expression of c fos pr otein in the rat plantar region was detected with immunohistochemical method. OFQ 20 μL, 50 μg/mL was injected into the lateral ventricle of the rat brain. Results: ① In RA rats, the pain threshold in A, B, D and E groups was lowered significantly, while after EA treatment, the pain threshold values, particularly on the 3rd, 4t h and 5th day, were increased significantly (P<0.01). There were no si gnificant differences between model+ OFQ+EA and RA model groups in the pain thre shold (P>0 .05), suggesting an antagonizing effect of OFQ on EA analgesia. ② In comparison with normal control group, the positive neurons of c fos expression in A (82.5 4±24.64) and B (174.87±38.23), D (168.42±34.75) and E (99.65±25.36) grou ps w ere increased considerably in comparison with group C (0.00±0.00), showing a st riking increase of c fos expression. The c fos positive neuron numbers in A a nd D groups were significant lower than that of B and D groups (P< 0.01), display ing that EA can significantly suppress RA induced c fos expression while this effect of EA is antagonized by intraventricular injection of OFQ.