Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

• Main Authors: Xiao-Yuan Mao, Dan-Feng Cao, Xi Li, Ji-Ye Yin, Zhi-Bin Wang, Ying Zhang, Chen-Xue Mao, Hong-Hao Zhou, Zhao-Qian Liu
• Format: Article
• Language: English
• Published: MDPI AG 2014-05-01
• Series: International Journal of Molecular Sciences
• Subjects: huperzine A; diabetes-associated cognitive decline; brain-derived neurotrophic factor; oxidative stress; inflammation; apoptosis
• Online Access: http://www.mdpi.com/1422-0067/15/5/7667

The present study was designed to probe the effects of Huperzine A (HupA) on diabetes-associated cognitive decline (DACD) using a streptozotocin (STZ)-injected rat model. Diabetic rats were treated with HupA (0.05 and 0.1 mg/kg) for seven weeks. Memory functions were evaluated by the water maze test. Nissl staining was selected for detecting neuronal loss. Protein and mRNA levels of brain-derived neurotrophic factor (BDNF) were analyzed by ELISA and real-time PCR, respectively. The activities of choline acetylase (ChAT), Acetylcholinesterase (AChE), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), NF-κB p65 unit, TNF-α, IL-1β, IL-6 and caspase-3 were measured using corresponding kits. After seven weeks, diabetic rats exhibited remarkable reductions in: body weight, percentage of time spent in target quadrant, number of times crossing the platform, ChAT and BDNF levels, SOD, GSH-Px and CAT accompanied with increases in neuronal damage, plasma glucose levels, escape latency, mean path length, AChE, MDA level as well as CAT, NF-κB p65 unit, TNF-α, IL-1β, IL-6 and caspase-3 in cerebral cortex and hippocampus. Supplementation with HupA significantly and dose-dependently reversed the corresponding values in diabetes. It is concluded that HupA ameliorates DACD via modulating BDNF, oxidative stress, inflammation and apoptosis.