Oxidative stress induced by β-amyloid peptide in pathogenesis of Alzheimer's disease in rats

AIM To investigate whether oxidative stress path way takes part in the whole process formation of Alzheimer's disease (AD). METHODS The AD rat's model was established by injection of beta amyloid peptide (β AP 1 40 , 10 μg) into cerebral ventricular system. CAT, T AOC, ChE level and consecutive changes (1, 2, 3 wk after injection) in brain tissue and peripheral blood were tested. RESULTS CAT, T AOC, ChE level in brain tissue was significantly decreased at 1 wk than that of control group (10.1±4.1), (6.8±0.8) and (3.4±1.0) kU·g -1 ( P 0.01). ChE, CAT and T AOC were more decreased (6.5±4.4), (2.0±1.2) and (2.4±1.2) kU·g -1 ( P 0.01). There is a positive relation between them and memory impairment. However, no changes of ChE and CAT in peripheral blood ( P 0.05), T AOC level decreased from 1 wk to 3 wk [(6.8±1.2) kU·g -1 , P 0.01 ]. CONCLUSION β AP could evoke oxidative stress, which plays an important role and a key factor in AD formation.