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Open AccessArticle

Stachys sieboldii Extract Supplementation Attenuates Memory Deficits by Modulating BDNF-CREB and Its Downstream Molecules, in Animal Models of Memory Impairment

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Department of Food Science and Human Nutrition, Chonbuk National University, 664-14 Duckjin-dong, Jeonju, Jeonbuk 561-756, Korea
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Division of Functional Food and Nutrition, Department of Agrofood Resources, National Institute of Agricultural Science, Rural Development Administration, Wanju 55365, Korea
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Department of Oral Physiology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561-756, Korea
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Author to whom correspondence should be addressed.
Nutrients 2018, 10(7), 917; https://doi.org/10.3390/nu10070917
Received: 8 May 2018 / Revised: 13 July 2018 / Accepted: 16 July 2018 / Published: 17 July 2018
Cholinergic dysfunction, impaired brain-derived neurotrophic factor and cAMP response element binding protein (BDNF-CREB) signaling are one of the major pathological hallmarks of cognitive impairment. Therefore, improving cholinergic neurotransmission, and regulating the BDNF-CREB pathway by downregulating apoptosis genes is one strategy for inhibiting the etiology of dementia. This study evaluates the potential effects of Stachys sieboldii MIQ (SS) extract against cognitive dysfunction and its underlying mechanisms. SS supplementation for 33 days improved scopolamine-induced memory impairment symptoms in Morris water maze test and Y-maze test. SS reduced the acetylcholineesterase activity and significantly increase acetylcholine and cholineacetyltransferase activity in the brain. In the subsequent mechanism study, SS regulated the mRNA expression level of neuronal plasticity molecules such as (nerve growth factor) NGF, BDNF, CREB, and its downstream molecules such as Bcl-2 and Egr-1 by downregulating the neuronal apoptosis targets in both hippocampus and frontal cortex. Additionally, inward currents caused by SS in hippocampal CA1 neurons was partially blocked by the GABA receptor antagonist picrotoxin (50 μM), suggesting that SS acts on synaptic/extrasynaptic GABAA receptors. These findings indicate that SS may function in a way that is similar to nootropic drugs by inhibiting cholinergic abnormalities, and neuronal apoptosis targets and ultimately increasing the expression of BDNF-CREB. View Full-Text
Keywords: Stachys sieboldii; dementia; memory loss; cholinergic neurotransmission; neuroplasticity targets; GABAA receptor Stachys sieboldii; dementia; memory loss; cholinergic neurotransmission; neuroplasticity targets; GABAA receptor
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MDPI and ACS Style

Ravichandran, V.A.; Kim, M.; Han, S.K.; Cha, Y.S. Stachys sieboldii Extract Supplementation Attenuates Memory Deficits by Modulating BDNF-CREB and Its Downstream Molecules, in Animal Models of Memory Impairment. Nutrients 2018, 10, 917.

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