【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1 5月龄健康雌性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[按体质量2.5 g/(kg·d)给予二十碳五烯酸灌胃,共6周],观察大鼠跳台潜伏时间及错误次数,同时测定大鼠海马组织总SOD活力和MDA含量。结果与痴呆模型组比较,ω-3多不饱和脂肪酸治疗组大鼠的跳台潜伏时间明显延长[分别为(230.88±29.35)s与(189.26±31.42)s](P<0.01),触电错误次数减少[分别为(7.3±2.2)次与(9.6±2.2)次](P<0.05),同时其大鼠海马组织总SOD活力增加[分别为(70.19±12.85)U/mg prot与(50.47±14.99)U/mg prot]和MDA含量减少[分别为(7.77±1.57)nmol/mg prot与(9.39±1.44)nmol/mg prot](P<0.05)。结论ω-3多不饱和脂肪酸可改善大鼠学习记忆能力,保护脑组织免遭自由基攻击,在一定程度上为临床治疗老年痴呆提供了实验基础。更多还原

【Abstract】 Objective To investigate the mechanism of ωo-3 polyunsaturated fatty acids in senile dementia. Methods The normal 15 months old Wistar rats were randomly divided into the normal control, model group and ω-3 polyunsaturated fatty acids group [EPA 2.5 g/(kg · d) by intragastric administration for 6 weeks]. The escape latency time and mistaken times were evaluated by using the step down test. The content of malondialdehyde (MDA) and superoxide dismutase (SOD) of the hippicampus tissue in rats were detected. Results Compared with the model group, ωo 3 polyunsaturated fatty acids group had lingeringly latency [(230.88 ±29.35)s vs. (189.26±31.42)s] (P<0.01) and less error times [(7.3±2.2)times vs. (9.6±2.2)times](P< 0.05). At the same time, ω-3 polyunsaturated fatty acids increased SOD [(70.19±12.85)U/mg prot vs. (50.47 ± 14.99)U/mg prot] and down regulated MDA of the hippicampus in rats [(7.77 ±1.57)nmol/mg prot vs. (9.39±1.44)nmol/mg prot] (P<0.05). Conclusions ω-3 polyunsaturated fatty acids could improve learning- memory function in rats and protect cerebral tissue against free radical. Also provides the experimental base of treatment with senile dementia.更多还原