Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats
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...
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Molecular Diversity Preservation International (MDPI)
2014
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057698/ |
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pubmed-40576982014-06-16 Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats Mao, Xiao-Yuan Cao, Dan-Feng Li, Xi Yin, Ji-Ye Wang, Zhi-Bin Zhang, Ying Mao, Chen-Xue Zhou, Hong-Hao Liu, Zhao-Qian Article 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. Molecular Diversity Preservation International (MDPI) 2014-05-05 /pmc/articles/PMC4057698/ /pubmed/24857910 http://dx.doi.org/10.3390/ijms15057667 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Mao, Xiao-Yuan Cao, Dan-Feng Li, Xi Yin, Ji-Ye Wang, Zhi-Bin Zhang, Ying Mao, Chen-Xue Zhou, Hong-Hao Liu, Zhao-Qian |
spellingShingle |
Mao, Xiao-Yuan Cao, Dan-Feng Li, Xi Yin, Ji-Ye Wang, Zhi-Bin Zhang, Ying Mao, Chen-Xue Zhou, Hong-Hao Liu, Zhao-Qian Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
author_facet |
Mao, Xiao-Yuan Cao, Dan-Feng Li, Xi Yin, Ji-Ye Wang, Zhi-Bin Zhang, Ying Mao, Chen-Xue Zhou, Hong-Hao Liu, Zhao-Qian |
author_sort |
Mao, Xiao-Yuan |
title |
Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
title_short |
Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
title_full |
Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
title_fullStr |
Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
title_full_unstemmed |
Huperzine A Ameliorates Cognitive Deficits in Streptozotocin-Induced Diabetic Rats |
title_sort |
huperzine a ameliorates cognitive deficits in streptozotocin-induced diabetic rats |
description |
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. |
publisher |
Molecular Diversity Preservation International (MDPI) |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057698/ |
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1612101390084079616 |