大鼠脑内δ-阿片受体在累加电针抗缺血性脑损伤中的作用  

Role of Intracerebral δ-opium Receptors in Protecting Ischemic Injury in Rats by Cumulative Electro-acupuncture

作　　者：田雪松[1,2] 周飞[1,3] 杨茹[1] 夏萤[3,4] 吴根诚[1] 郭景春[1] 

机构地区：[1]复旦大学上海医学院中西医结合系,医学神经生物学国家重点实验室,上海200032 [2]上海中医药大学药物安全评价研究中心,上海201203 [3]上海市针灸经络研究中心 [4]美国耶鲁大学医学院

出　　处：《上海中医药杂志》2008年第6期71-74,共4页Shanghai Journal of Traditional Chinese Medicine

基　　金：国家重大基础研究计划("973"计划)专项基金资助项目(2005CB523306);国家自然科学基金资助项目(30672721);上海市科委科研基金资助项目(06DZ19734;04DZ19836;05DZ19745);复旦大学第6批研究生创新基金资助项目;美国国立卫生研究院(NIH)基金项目(HD-34852)

摘　　要：目的探讨δ-阿片受体(DOR)在累加电针抗脑缺血损伤中的作用。方法大鼠随机分为7组:假手术组、单纯脑缺血组、脑缺血+电针组、脑缺血+假电针组、脑缺血+TAN-67(DOR激动剂)组、脑缺血+naltrindole(DOR拮抗剂)组、脑缺血+naltrindole+电针组。除假手术组外,其余各组均用大脑中动脉线栓法致大鼠局部脑缺血再灌注,缺血1 h再灌7 d。于缺血前30 min及再灌第2、4、5、6、7天,侧脑室注射naltrindole或TAN-67;于再灌开始及第2、4、5、6、7天,电针"水沟"和"内关"穴30 min。再灌后24 h评测神经功能缺损程度,再灌第7天后检测脑梗死体积。结果脑缺血+电针组或脑缺血+TAN-67组与单纯脑缺血组相比梗死体积减小、神经功能缺损减轻(P<0.05);脑缺血+naltrindole组与单纯脑缺血组相比梗死体积增大、神经功能缺损加剧(P<0.05);脑缺血+naltrindole+电针组与累加电针组相比,梗死体积增大、神经功能缺损评分加剧(P<0.05);假电针组与单纯脑缺血组相比梗死体积、神经功能缺损评分无显著性差异(P>0.05)。结论DOR拮抗剂naltrindole能够翻转累加电针对缺血/再灌大鼠的神经保护作用,提示其活动可能是累加电针抗脑缺血损伤中的重要机制。Objective This study was carried out to assess the role of 8-opioid receptors （DOR） in protection against ischemic injury by electro-acupuncture （EA）. Methods The rats were randomly divided into 7 groups： sham group, ischemia group, ischemia ＆ EA group, ischemia ＆ sham group, ischemia ＆ TAN-67 （DOR agonist） group, ischemia ＆ nahrindole （DOR antagonist） group and ischemia ＆naltrindole ＆ EA group. Transient （1h） focal cerebral ischemia was induced by middle cerebral artery occlusion （MCA0）. EA was applied to Shuigou （GV 26） and Neiguan （PC 6） for 30 rain starting immediately after the onset of reperfusion and repeated （30 min, once a day） on days 2, 4, 5, 6 and 7 after reperfusion. Drugs （TAN-67 or naltrindole） or artificial cerebral spinal fluid was injected to the lateral cerebral ventricle 30 min before ischemia and on the 2nd, 4th, 5th, 6th and 7th days after reperfusion. Neurological deficit scores were assessed 24h after reperfusion. Cerebral infarction was measured on the 7th day after reperfusion. Results Both ischemia ＆ EA group and ischemia ＆ TAN-67 group significantly reduced infarct volume and attenuated neurological deficits （P 〈 0.05）, while sham EA did not induce any protective effect. Ischemia ＆ naltrindole group significantly enlarged total infarct volume and exacerbated neurological deficits. lschemia ＆ naltrindole ＆ EA group completely abolished the EA-induced protection from ischemic infarction and neurological deficits. Conclusion DOR antagonist naltrindole can reverse the neuroprotective effect of cumulative EA on cerebral ischemia, suggesting that DOR plays an important role in the EA-induced brain protection against ischemic injury.

关 键 词：电针 脑缺血 δ-阿片受体:δ-阿片受体拮抗剂 δ-阿片受体激动剂 

分 类 号：R245.97[医药卫生—针灸推拿学]