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Int. J. Mol. Sci. 2014, 15(5), 7667-7683; doi:10.3390/ijms15057667
Article

Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats

1,2,†
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3,†
,
1,2
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1,2
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4
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1,2
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1,2
,
1,2
 and
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 These authors contributed equally to this work.
* Author to whom correspondence should be addressed.
Received: 24 February 2014 / Revised: 15 April 2014 / Accepted: 17 April 2014 / Published: 5 May 2014
(This article belongs to the Section Biochemistry, Molecular Biology and Biophysics)
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Abstract

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.
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
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
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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.

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