双苯氟嗪对氯化铝致痴呆大鼠学习记忆的改善作用及机制

目的观察双苯氟嗪(dipfluzine)对氯化铝致痴呆大鼠学习记忆能力的影响并分析其机制。方法采用腹腔注射氯化铝制备痴呆大鼠模型,灌胃给予2个剂量双苯氟嗪(3.0和10.0mg/kg)60天,跳台仪测定大鼠学习记忆能力,生化分析法测定大鼠脑组织超氧化物歧化酶(superoxidedismutase,SOD)、丙二醛(malondialdehyde,MDA)和总抗氧化能力(totalantioxidativecapacity,T AOC)。结果学习记忆测试结果显示,除记忆测试中双苯氟嗪3.0mg/kg对错误次数无明显影响外,2个剂量均可缩短模型动物的反应时间及累积电击时间,延长跳台潜伏期,减少错误次数,且均有统计学意义(P<0.05,P<0.01)。生化指标测定显示,双苯氟嗪10.0mg/kg可显著增强模型动物脑组织中SOD活力和T AOC,降低MDA的含量,且均有统计学意义(P<0.05,P<0.01);双苯氟嗪3.0mg/kg组脑组织中MDA含量较模型对照组明显降低(P<0.05),SOD和T AOC亦有升高趋势,但无统计学意义(P>0.05)。2剂量组各指标间无统计学意义(P>0.05)。结论双苯氟嗪对氯化铝致痴呆大鼠的学习记忆障碍有明显改善作用,这种改善作用可能与其抗脂质过氧化作用有关。

IMPROVEMENT OF DIPFLUZINE ON LEARNING AND MEMORY IN DEMENTIA RAT INDUCED BY AlCl3 AND ITS MECHANISM

ObjectiveTo study the effects of dipfluzine on learning and memory ability in dementia rats induced by aluminum chloride and its mechanism. MethodsDementia model in rats was induced by intraperitoneal injection with aluminum chloride. Dipfluzien ( 3.0 and 10.0 mg/kg) was given by oral administration for 60 days. The step-down avoidance test was used to observe learning and memory ability of rats. Biochemisty method was used to determine the activities of superoxide dismutase(SOD), total antioxidative capacity(T-AOC) and the content of malondialdehyde(MDA) in the brain tissue. ResultsIn learning and memory test, after model rats were treated by oral administration of dipfluzine ( 3.0 and 10.0 mg/kg), the reactive time and the time of stimulation were shortened, the step down latency was prolonged and the number of errors was reduced (P< 0.05, P< 0.01), while dipfluzine 3.0 mg/kg could not reduced the number of errors in the memory test. Dipfluzine 10.0 mg/kg increased the activities of SOD and T-AOC in the brain tissue significantly, and decreased the content of MDA, while dipfluzine 3.0 mg/kg could decrease the content of MDA only (P< 0.05, P< 0.01) in the brain tissue. But there was no difference between every index of the two dosage of dipfluzine(P> 0.05). ConclusionDipfluzine has an effect of improving learning and memory ability of dementia model rats induced by aluminum chloride, which is possibly due to the antagonisic effect on lipid peroxidation.