中文摘要：

有重复 electroacupuncture (EA ) 的背景 Preconditioning 能模仿 ischemic preconditioning 在老鼠导致服的 ischemic 忍耐。现在的学习被设计调查是否mu()，delta()-或kappa() -opioid 受体涉及老鼠是的重复 EA preconditioning.Methods 导致的 neuroprotection 有 naltrindole ( NTI )的 pretreated ， nor-binaltorphimine ( nor-BNI )或 D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 ( CTOP )，它是一高度选择，-或 -opioid 受体对手分别地，在每 EA preconditioning 前( 30 每天纪录， 5 天)。在最后 EA 处理以后的 24 个小时，中间的服的动脉吸藏(MCAO ) 被导致 120 分钟。大脑梗塞体积与 2,3,5-triphenyltetrazolium 氯化物在仅仅收到了 EA preconditioning 的老鼠在 MCAO 以后并且与那相比在 24 个小时染色被决定。在另一个实验，在老鼠大脑的 met-enkephalin-like immunoreactivity 被 immunohistochemistry 在 EA preconditioning 减少了的 EA preconditioning 和控制 rats.Results 调查大脑梗塞体积与控制老鼠(P=0.000 ) 相比。NTI 和 CTOP 的管理稀释了 EA preconditioning 导致的大脑梗塞体积减小，与在 EA preconditioning 老鼠(P0.001 ) 的比那的更大的梗塞体积介绍。但是 nor-BNI 管理没堵住 EA preconditioning 导致的梗塞卷减小，比控制组老鼠(P=0.000 ) 与更小的梗塞体积介绍。met-enkephalin-like immunoreactivity 的数字在 EA preconditioning 老鼠的积极神经原是多于控制老鼠(P=0.000 ) ， .Conclusion 重复了 EA preconditioning，这刺激 enkephalins 的版本，它可以绑 - 并且对焦点的服的局部缺血导致忍耐的 -opioid 受体。

英文摘要：

Background Preconditioning with repeated electroacupuncture （EA） could mimic ischemic preconditioning to induce cerebral ischemic tolerance in rats. The present study was designed to investigate whether mu（μ）-, delta（δ）- or kappa（κ）-opioid receptors are involved in the neuroprotecUon induced by repeated EA preconditioning. Methods The rats were pretreated with naltrindole （NTI）, nor-binaltorphimine （nor-BNI） or D-Phe-Cys-Tyr-D- Trp-Om-Thr-Pen-Thr-NH2 （CTOP）, which is a highly selective δ-, κ- or μ-opioid receptor antagonist respectively, before each EA preconditioning （30 minutes per day, 5 days）. Twenty-four hours after the last EA treatment, the middle cerebral artery occlusion （MCAO） was induced for 120 minutes. The brain infarct volume was determined with 2,3,5-tdphenyltetrazolium chloride staining at 24 hours after MCAO and compared with that in rats which only received EA preconditioning. In another experiment, the met-enkephalin-like immunoreactivity in rat brain was investigated by immunohistochemistry in both EA preconditioning and control rats. Results The EA preconditioning reduced brain infarct volume compared with the control rats （P=-0.000）. Administration of both NTI and CTOP attenuated the brain infarct volume reduction induced by EA preconditioning, presenting with larger infarct volume than that in the EA preconditioning rats （P〈0.001）. But nor-BNI administration did not block the infarct volume reduction induced by EA preconditioning, presenting with smaller infarct volume than the control group rats （P=-0.000）. The number of met-enkephalin-like immunoreactivity positive neurons in the EA preconditioning rats was more than that of the control rats （P=-0.000）. Conclusion Repeated EA preconditioning stimulates the release of enkephalins, which may bind 5- and p-opioid receptors to induce the tolerance against focal cerebral ischemia.