纳络酮对AlCl3致急性衰老小鼠记忆障碍的保护作用及机制研究

目的 研究纳络酮对A1Cl3所致急性衰老小鼠记忆障碍的保护作用及其机制。方法 皮下注射A1Cl3 70mg/kg共7d，腹腔注射纳络酮0．1、0．3、0．9mg/kg共7d后，用跳台、避暗等实验方法测定小鼠学习记忆能力，同时测定小鼠肝丙二醛(MDA)、脑B型单胺氧化酶(MAO—B)的含量。结果 A1C13中毒小鼠记忆能力明显降低，表现为避暗、跳台实验的错误次数明显增加，以及增加肝丙二醛和脑B型单胺氧化酶的作用。纳络酮各剂量组能够减少小鼠电击次数(错误次数)，24h重复实验，可延长跳下平台的潜伏期及进入暗箱的潜伏期，错误次数明显减少；同时降低了肝MDA和MAO—B。结论 纳络酮对A1Cl3所致急性衰老小鼠记忆障碍具有保护作用，能增强学习记忆能力。其作用机制可能和降低MAO—B、清除过氧化脂质作用有关。

Protective effects and mechanism of naloxone on the learning and memory of mouse with acute senescent model induced by AlCl3

Objective To study the protective effects and mechanism of naloxone on the learning and memory of mouse with acute senescent model induced by AlCl 3.Methods After sc AlCl 3 70mg/kg for 7d and ip 0.1, 0.3,0.9 mg/kg for 7d,the ability of learning and memory of mouse was examined using step down test and step through test and the levels of MDA in liver and MAO B in brain were measured. Results Naloxone could reduce the number of electric stroke and stroke mice, prolong latency of mouse's step down and latency of enterning dark cabin,reduce wrong times and frequency after 24 hours impairing activities of liver's MDA and brain's MAO B. Conclusion Naloxone has protective effects on the learning and memory of mouse with acute senescent model induced by AlCl 3. Its mechanism might be due to impairing the activities of the liver's MDA and brain's MAO B.