摘要
目的:观察电针对完全弗氏佐剂(CFA)致炎性痛大鼠急性期脊髓背角细胞外信号转导激酶1/2(ERK1/2)磷酸化水平的影响,探讨电针即刻镇痛效应的部分细胞信号转导机制。方法:雄性健康SD大鼠53只,分两批进行实验。第1批实验大鼠23只,全部采用CFA造模,观察CFA致炎对大鼠痛阈的影响,并用免疫组化法检测大鼠患侧脊髓背角p-ERK1/2阳性细胞的表达情况。第2批实验大鼠30只,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),每组各10只。CFA组和EA组大鼠采用CFA造模,EA组大鼠造模后5.5h予电针治疗1次。观察电针对CFA大鼠的即刻镇痛效应及其对大鼠脊髓背角p-ERK1/2阳性细胞表达的干预作用。结果:第1批实验大鼠:造模后5h,CFA大鼠痛阈显著降低(P<0.01),造模后3d、7d、14d3个时点,CFA大鼠痛阈均显著低于造模前(均P<0.01);但p-ERK1/2阳性细胞主要集中在造模后5h表达,并于造模后3d恢复正常。第2批实验大鼠:CFA造模成功诱导CFA组和EA组大鼠痛阈降低,与同期N组大鼠相比差异有统计学意义(均P<0.01)。接受1次电针治疗后,EA组大鼠痛阈明显提高(P<0.01),并显著高于同期CFA组(P<0.01)。造模后6h,CFA组大鼠腰段脊髓背角p-ERK1/2阳性细胞表达增多(P<0.01),而EA组则明显减少(P<0.01)。结论:抑制炎性痛大鼠腰段脊髓背角ERK1/2活化,可能是电针发挥即刻镇痛效应的关键细胞信号转导机制之一。
Objective To observe influence of electroacupuncture（EA） on phosphorylation of extracellular signal-regulated kinases 1/2（ERK1/2） in spinal cord dorsal horn（SCDH） in rats with acute inflammatory pain induced by complete Freund＇s adjuvant（CFA）,further elucidate the immediate analgesic mechanism of EA via cellular signal transduction.Methods Fifty-three healthy male SD rats were divided into two batches.The inflammatory pain models of the first batch of 23 rats were established by using CFA.The changes of the paw withdrawal thresholds（PWTs） of rats were observed and positive cells of p-ERK1/2 in affected SCDH were detected by using immunohistochemistry method.The second batch of 30 rats were randomly divided into a blank control group（N group）,CFA group and EA group,10 rats in each group.The rats of CFA group and EA group were induced inflammatory pain by using CFA,and the EA group was treated with EA at 5.5 h after the model establishment.The changes of PWTs and the positive cells of p-ERK1/2 in SCDH were observed.Results The PWTs of the first batch of rats obviously decreased at 5 h,3 d,7 d and 14 d after CFA administration（all P0.01）.However,the p-ERK1/2 positive cells in affected SCDH only increased at 5 h after CFA-injection and returned to normality at 3 d after the model establishment.In the second batch,compared with that of N group at the same time point,PWTs of rats in both CFA and EA group obviously decreased after the model establishment（both P0.01）.PWTs of rats in EA group which accepted EA treatment once were longer than those before EA treatment and corresponding PWTs in CFA group at the same time point（both P0.01）.Moreover,the numbers of p-ERK1/2 positive cells of affected SCDH increased significantly in CFA group at 6 h after the model establishment（P0.01）,however,which were decreased significantly in EA group（P0.01）.Conclusion Inhibiting ERK1/2 activation of SCDH may be one of the pivotal mechanism of cellular signal transduction of the immediate analgesic effect educed by EA.
出处
《中国针灸》
CAS
CSCD
北大核心
2012年第11期1007-1011,共5页
Chinese Acupuncture & Moxibustion
基金
国家自然科学基金资助项目30873305
浙江省自然基金资助项目:Y2091151
浙江省"重中之重"学科(针灸推拿学)建设经费资助项目:浙教高科[2008]255号
关键词
镇痛
电针
细胞外信号转导激酶
Analgesic
Electroacupuncture
Extracellular Signal-Regulated Kinase
