摘要目的 探讨ω-3多不饱和脂肪酸治疗老年痴呆的可能机制.方法 将15月龄雌性健康Wistar大鼠随机分为对照组、痴呆模型组和ω-3多不饱和脂肪酸治疗组(EPA 2.5g·kg-1·d-1灌胃,共6周).观察大鼠跳台潜伏时间及错误次数,测定大鼠血清前列腺素E(PGE2)含量,脑组织花生四烯酸(AA)、二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)的改变.结果 跳台潜伏时间和触电错误次数在对照组大鼠中[分别为(264.83±16.99)s,(4.8±1.7)次]、痴呆模型组大鼠中[分别为(189.26±31.42)s,(9.6±2.2)次]和治疗组大鼠中[分别为(230.88±29.35)s,(7.3±2.2)次],差异有显著性(分别为F=20.114,F=13.638,P=0.000).痴呆模型组大鼠与对照组大鼠比较,跳台潜伏时间缩短(LSD-t=6.332,P=0.000)和触电错误次数增加(LSD-t=5.221,P=0.000).与痴呆模型组比较,ω-3多不饱和脂肪酸能明显延长老年痴呆大鼠的跳台潜伏时间(LSD-t=3.487,P=0.002)、减少触电错误次数(LSD-t=2.502,P =0.019).大鼠血清PGE2水平在对照组、痴呆模型组、治疗组,差异有显著性(F=6.851,P=0.004).痴呆模型组大鼠血清PGE2明显比对照组升高(LSD-f=3.684,P=0.001),ω-3多不饱和脂肪酸可降低痴呆大鼠血清PGE2含量(LSD-t=2.152,P=0.041).大鼠脑AA、EPA、DHA在对照组中、痴呆模型组中、治疗组大鼠中.差异有显著性(分别为F=5.538、P=0.010,F=4.240、P=0.025,F=4.633、P=0.019).ω-3多不饱和脂肪酸可降低痴呆大鼠脑组织AA(LSD-t=2.273,P=0.031),升高EPA和DHA含量(分别为LSD-t=2.428、P=0.022,LSD-t=2.520,P=0.018).结论 ω-3多不饱和脂肪酸可以提高大鼠学习记忆能力,改变脑组织AA、EPA和DHA的构成比,防止老年痴呆的发生.

abstractsObjective To investigate the mechanism of ω-3 polyunsaturated fatty acids in senile dementi-a. Methods The normal 15 months old Wistar rats were randomly divided into normal control,model group andre-cape latency time and mistaken times were evaluated by using the step down test. The content of serum PGE2 and urachidonic acid(AA),EPA and DHA of cerebral tissue in rats were detected. Results The lingeringly latency and error times were ( 264.83±16.99) s and (4.8±1.7) times in control group, ( 189.26±31.42)s and ( 9.6± 2.2) times in model group, (230.88±29.35) s and (7.3±2.2) times in treatment group, respectively. Differences in three groups were very significantly by analyses of variance(F=20.114, F=13.638, P=0.000). Compared with model group, control group and treatment group had lingeringly latency(LSD-t=6.332,P=0.000 and LSD-t =3.987, P=0.002, respectively) and less error times (LSD-t=5.221, P=0.000 and LSD-t=3.502, P= 0.019,respectively). Serum PGE2 were in control group, model group and treatment group were very significantly by analyses of variance(F=6.851 , P=0.004). Compared with model group,control group had less serum PGE2 (LSD-t=3.684, P=0.001 ). Compared with model group,ω-3 polyunsaturated fatty acids chould decrease serum PGE2( LSD-t=2.152, P=0.041 ). AA, EPA and DHA of cerebral tissue in control group, in model group, in treatment group, respectively. Differences in three groups were very significantly by analyses of variance (F=5.538, P=0.010, F=4.240, P=0.025, F=4.633, P=0.019). Compared with model group,ω-3 polyunsaturat-ed fatty acids could decrease A A(LSD-t=2.273, P=0.031) and increase EPA and D HA (LSD-t=2.428, P= 0.022,LSD-t=2.520, P=0.018,respectively). Conclusions ω-3 polyunsaturated fatty acids can improve learning-memory function in rats,change the proportion of AA,EPA and DHA in cerebral tissue and prevent senile dementia.