Puerarin attenuates learning and memory impairments and inhibits oxidative stress in STZ-induced SAD mice

• Published in: Neurotoxicology (Park Forest South) 2015-12, Vol.51, p.166-171
• Main Authors: Zhao, Shan-shan, Yang, Wei-na, Jin, Hui, Ma, Kai-ge, Feng, Gai-feng
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - chemically induced; Alzheimer Disease - metabolism; Alzheimer Disease - psychology; Alzheimer's disease; Animals; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Disease Models, Animal; Female; Glutathione Peroxidase - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Isoflavones - administration & dosage; Learning - drug effects; Learning and memory; Malondialdehyde - metabolism; Maze Learning - drug effects; Memory - drug effects; Mice; Oxidative stress; Oxidative Stress - drug effects; Pueraria lobata; Puerarin; Streptozocin; Streptozotocin; Superoxide Dismutase - metabolism
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2015.10.010

•ICV injection of STZ induced learning and memory deficits and oxidative stress in mice.•Puerarin could attenuate learning and memory impairments in SAD mice.•Puerarin had effects on inhibiting oxidative stress in SAD mice.•Purerarin may be a promising therapeutic agent to AD. Puerarin (PUE), an isoflavone purified from the root of Pueraria lobata (Chinese herb), has been reported to attenuate learning and memory impairments in the transgenic mouse model of Alzheimer's disease (AD). In the present study, we tested PUE in a sporadic AD (SAD) mouse model which was induced by the intracerebroventricular injection of streptozotocin (STZ). The mice were administrated PUE (25, 50, or 100mg/kg/d) for 28 days. Learning and memory abilities were assessed by the Morris water maze test. After behavioral test, the biochemical parameters of oxidative stress (glutathione peroxidase (GSH-Px), superoxide dismutases (SOD), and malondialdehyde (MDA)) were measured in the cerebral cortex and hippocampus. The SAD mice exhibited significantly decreased learning and memory ability, while PUE attenuated these impairments. The activities of GSH-Px and SOD were decreased while MDA was increased in the SAD animals. After PUE treatment, the activities of GSH-Px and SOD were elevated, and the level of MDA was decreased. The middle dose PUE was more effective than others. These results indicate that PUE attenuates learning and memory impairments and inhibits oxidative stress in STZ-induced SAD mice. PUE may be a promising therapeutic agent for SAD.