Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

International Journal of Molecular Sciences

Xiao-Yuan Mao¹  Dan-Feng Cao²  Xi Li¹  Ji-Ye Yin¹  Zhi-Bin Wang³  Ying Zhang¹  Chen-Xue Mao¹  Hong-Hao Zhou¹ 

[1] Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha 410078, China; E-Mails:;Department of Genetics, Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Kunming 650118, China; E-Mail:;School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China; E-Mail:

关键词: huperzine A;    diabetes-associated cognitive decline;    brain-derived neurotrophic factor;    oxidative stress;    inflammation;    apoptosis;   

DOI  :  10.3390/ijms15057667

来源: mdpi

【 摘 要 】

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.

【 授权许可】

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