Next Article in Journal
Different Role of Tumor Necrosis Factor-α Polymorphism in Non-Hodgkin Lymphomas among Caucasian and Asian Populations: A Meta-Analysis
Previous Article in Journal
Molecular Modelling Study of the PPARγ Receptor in Relation to the Mode of Action/Adverse Outcome Pathway Framework for Liver Steatosis
Open AccessArticle

Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

by Xiao-Yuan Mao 1,2,†, Dan-Feng Cao 3,†, Xi Li 1,2, Ji-Ye Yin 1,2, Zhi-Bin Wang 4, Ying Zhang 1,2, Chen-Xue Mao 1,2, Hong-Hao Zhou 1,2 and Zhao-Qian Liu 1,2,*
1
Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha 410078, China
2
Institute of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, China
3
Department of Genetics, Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Kunming 650118, China
4
School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2014, 15(5), 7667-7683; https://doi.org/10.3390/ijms15057667
Received: 24 February 2014 / Revised: 15 April 2014 / Accepted: 17 April 2014 / Published: 5 May 2014
(This article belongs to the Section Biochemistry)
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. View Full-Text
Keywords: huperzine A; diabetes-associated cognitive decline; brain-derived neurotrophic factor; oxidative stress; inflammation; apoptosis huperzine A; diabetes-associated cognitive decline; brain-derived neurotrophic factor; oxidative stress; inflammation; apoptosis
MDPI and ACS Style

Mao, X.-Y.; Cao, D.-F.; Li, X.; Yin, J.-Y.; Wang, Z.-B.; Zhang, Y.; Mao, C.-X.; Zhou, H.-H.; Liu, Z.-Q. Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats. Int. J. Mol. Sci. 2014, 15, 7667-7683.

Show more citation formats Show less citations formats

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop