【摘要】 目的 :初步研究保护蛋白对 D-半乳糖诱导的亚急性衰老小鼠的保护作用并探讨其机制。方法 :昆明鼠随机分成三组 ,模型组和保护组腹腔注射 D-半乳糖 12 0 mg/(Kg·d)诱导小鼠亚急性衰老 ,保护组同时注射保护蛋白 6mg/(Kg·d) ,对照组注射等量生理盐水。40 d后 ,处死小鼠 ,分别测定各组小鼠血清总 SOD活性 ,脑组织 MDA及脂褐素含量 ,并电镜观察小鼠大脑皮层神经元的超微结构。结果 :对照组、保护组小鼠的血清总 SOD活性明显高于模型组 (P<0 .0 5 ) ,脑组织 MDA和脂褐素含量显著低于模型组 (P<0 .0 5 ) ,而保护组与对照组的各项指标无显著性差异 (P>0 .0 5 )。电镜观察可见模型组小鼠次级溶酶体增多并有脂褐素沉积 ,线粒体有轻度肿胀 ;PRP保护组次级溶酶体增多但无脂褐素沉积 ,其它细胞器基本正常。结论 :保护蛋白对 D-半乳糖诱导的亚急性衰老小鼠有一定的保护作用更多还原

【Abstract】 OBJECTIVE:To study the effect of Protective Protein(PRP) on subacute aging model mice induced by D galactose. METHOD:Kunming mice were divided into three groups. The Control group was injected with normal saline, and the subacute aging model was induced by injection of D galactose 120mg/kg×d in mice. The mice of protection group were injected with activated PRP at a dose of 6mg/kg×d together with D galatcose treatment. After 40 days, mice were killed and parts brain were cut for histology fical examination. The activity of superoxide dismutase in serum and the contents of lipid peroxides in brain were measured by test kits. The contents of lipofuscin in brain were quantitated by fluorometry.RESULTS:Histological examination of brain showed that mice of model group has more remarkable aging characteristics than those of control and protection group. Furthermore, compared with control group and protection group, it showed that in model group the activity of superoxide dismutase decreased in serum; the contents of lipid peroxides and lipofuscin in brain both increased. CONCLUSION:PRP might delay aging process in mice induced by D galactose.更多还原