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作 者:魏伟[1] 沈玉先[1] 丁长海[1] 徐星铭[1] 刘泽源[1] 徐叔云[1]
机构地区:[1]安徽医科大学临床药理研究所
出 处:《中国药理学通报》1998年第1期72-74,共3页Chinese Pharmacological Bulletin
基 金:安徽省自然科学研究基金
摘 要:目的观察褪黑素(MT)对吗啡(Mor)致依赖性的作用及机制分析。方法连续ipMor与纳络酮催促建立小鼠依赖模型,甩尾法,淋巴细胞增殖反应和脑啡肽(Met-Enk)放免测定。结果Mor依赖组小鼠痛阈下降,跳跃次数增加,肛温降低,伴有胸腺细胞增殖能力的低下,Mor依赖小鼠的脑和血浆Met-Enk亦明显降低。本文首次发现igMT(30、90mg·kg-1×7d)能明显提高依赖性小鼠的痛阈,减少跳跃次数,恢复其肛温,阻止Mor对淋巴细胞功能的抑制,并能维持脑、血浆Met-Enk接近正常对照水平。结论MT具有对抗Mor致小鼠依赖性作用,其机制与维持内源性Met-Enk水平有关。AIM To observe the effects and mechanisms of melatonin (MT) on morphine (Mor)induced mice dependence. METHODS The Mordependentmice model was established by intraperitoneal (ip) administered Mor (10 mg·kg-1) for seven days and the pain threshold, thymocyte proliferation and methionineenkephalin(MetEnk) were determined by the tailflick, cell incubation and radioimmunoassay, respectively. RESULTS The pain threshold and the thymocytes proliferation in Mordependent mice were all decreased, and there were a marked increase in jumping number and a marked decrease in rectal temperature after naloxone (Nal) precipitation. The results also showed that the brain and plasma MetEnk levels were lower in Mordependent mice. MT(30,90 mg·kg-1,ig×7 d) could significantly antagonized the effects induced by Mor and maintained the brain and plasma MetEnk levels to normal status. CONCLUSIONS MT could antagonize the Morinduced mice dependence, which was related to its maintaining the levels of endogenous MetEnk.
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