Extract (EGb) Inhibits Oxidative Stress in Neuro 2A Cells Overexpressing APPsw.

Alzheimer's disease (AD) is a common neurodegenerative disease. Abundant evidence demonstrates that oxidative stress may be not only an early event in this disease, but also a key factor in the pathogenesis of AD. extract (EGb) has a strong ability to scavenge oxygen free radicals and supply hydrogen. The present study aims to investigate the effects of EGb on Neuro 2A cells transfected with Swedish mutant APP (APPsw). Stably transfected Neuro 2A cell lines expressing human wild-type APP (APP695), APPsw, or empty vector(neo) pEGFP-N2 were treated with 100 g/ml EGb for 0, 2, 4, 6, 8, and 10 h. Oxidative stress was assessed by measuring free radicals and the activities of antioxidant enzymes. Our studies showed that EGb treatment reduced the production of reactive oxygen species (ROS) and the levels of malondialdehyde (MDA) significantly while total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were enhanced in Neuro 2A cells overexpressing APPsw. Meanwhile, A levels in these cells were also reduced compared to the levels in untreated cells and control cells (empty vector(neo) pEGFP-N2). These findings suggest that EGb can reduce oxidative stress by decreasing free radical and enhancing antioxidant status, further leading to reduced A aggregation; EGb might be a potential therapeutic agent for Alzheimer's disease (AD).