电针上调δ阿片受体的表达减轻大鼠急性缺血性脑损伤  

Electroacupuncture protects the brain against acute ischemic injury via up-regulation of delta-opioid receptor in rats

作　　者：田雪松[1] 周飞[1] 杨茹[1] 夏萤[2] 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]上海市针灸经络研究中心

出　　处：《中西医结合学报》2008年第6期632-638,共7页Journal of Chinese Integrative Medicine

基　　金：国家973计划中医理论基础研究专项(No.2005CB523306);上海市科委基金资助项目(No.06DZ19734;04DZ19836;05DZ19745);复旦大学第六批研究生创新基金资助项目;美国国立卫生研究院(NIH)项目(No.HD-34852);国家自然科学基金资助项目(No.30672721)

摘　　要：目的:探讨δ-阿片受体(delta-opioid receptor,DOR)在电针抗急性脑缺血损伤中的作用。方法:51只大鼠随机分为假手术组、假电针组、模型组、电针组、DOR拮抗剂+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并行再灌注。电针于再灌注时开始,持续30min。再灌注24h后检查神经功能缺损程度、脑梗死体积。另取12只大鼠分为假手术组、模型组、电针组和DOR拮抗剂+电针组,蛋白印迹法检测脑组织中DOR蛋白的表达。结果:与模型组、假电针组比较,电针组脑梗死体积减小(P<0.05),神经功能缺损评分增加(P<0.05)。电针组60kD的DOR蛋白表达较模型组增加(P<0.05),36kD的DOR蛋白表达有增加趋势,但差异无统计学意义。DOR拮抗剂+电针组脑梗死体积、神经功能缺损评分与模型组和假电针组比较,差异无统计学意义,DOR蛋白表达和模型组比较,差异亦无统计学意义。结论:电针通过增加DOR的表达减轻缺血性脑梗死和神经功能缺损。Objective： To explore the effect of δ-opioid receptor （DOR） in electroacupuncture （EA） protecting the brain against acute ischemic injury. Methods： Fifty-one rats were randomly divided into sham ischemia group, ischemia group, sham EA group, EA group, and EA＋DOR antagonist （naltrindole） group. Transient focal cerebral ischemia （1 hour） was induced in rat brain by middle cerebral artery occlusion （MCAO） method. EA was applied on Shuigou （GV 26） and Neiguan （PC 6） for 30 min. starting immediately after the onset of reperfusion. Neurological deficit scores and volume of cerebral infarction were detected after 24-hour reperfusion. Other 12 rats were randomly divided into sham ischemia group, ischemia group, EA group and EA＋naltrindole group. DOR protein expressions were assessed by Western blotting after 24-hour reperfusion. Results： In comparison with the ischemia group and sham EA group, EA significantly reduced ischemic infarction and neurological deficits （P〈0.05）; EA significantly increased the expression of 60 kD DOR protein （P〈0.05） and tended to increase that of 36 kD DOR protein （P〉0.05）. When naltrindole was combined with EA, the naltrindole completely abolished the EA-induced protection in ischemic infarction and neurological deficits, and also arrested the expression of DOR. Conclusion： EA can up-regulate DOR expression and protect the brain from ischemia-reperfusion injury.

关 键 词：电针 短暂性脑缺血 阿片受体δ 大鼠 

分 类 号：R245.31[医药卫生—针灸推拿学]