摘要
观察外源性 β淀粉样蛋白 (β Amyloidpeptide ,Aβ) 2 5～ 35引起大鼠大脑的氧化应激。于大鼠侧脑室内一次性注射聚集态的Aβ(2 5～ 35 ) 15nmol后 ,5 ,9和 14d分别测定海马的脂质过氧化产物丙二醛 (malodialdehyde ,MDA)含量和还原型谷胱甘肽 (reducedglutathione,GSH)水平以及谷胱甘肽过氧化物酶 (glutathioneperoxidase,GSH PX)和超氧化物歧化酶 (Superoxidedismutase ,SOD)活性。与对照组相比 ,Aβ组大鼠术后 5d时MDA含量增加 (P <0 0 5 ) ,抗氧化酶GSH PX活性下降 (P <0 0 0 1) ,9d时GSH PX和SOD活性显著升高 (P <0 0 1和P <0 0 5 )。 14d时 ,两组间各个指标均无明显差别。结果表明在大鼠脑室内一次性注射Aβ(2 5～ 35 )可导致氧化应激反应 ,这一改变与时间相关 。
The study the oxidative stress induced by exogenous Aβ(25～35). Rats received intracerebroventricular administration of aggregated Aβ(25～35) 15nmol. On the day of 5, 9 and 14 postoperative (PD), the content of malodiadehyde (MDA) and reduced glutathione(GSH), as well as the activities of glutathione peroxidase (GSH PX) and superoxide dismutase(SOD) in hippocampus were measured. The MDA level increased significantly ( P <0.05) and activity of GSH PX decreased significantly ( P <0.001) in experimental rats on the 5 PD; both GSH PX and SOD activity increased significantly on the 9 PD ( P <0.01 and P <0.05) as compared with the control (vehicle). On the 14 PD, no difference was found in all the four parameters between the two groups. The results indicate that synthetic Aβ(25～35) can induce oxidative stress as a function of time in rat brain and it can be compensated by antioxidative system.
出处
《基础医学与临床》
CSCD
北大核心
2002年第5期466-468,共3页
Basic and Clinical Medicine
基金
国家 95攻关课题 (96 -C0 2 - 0 1- 0 9)
