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Beneficial Effects of Gagam-Palmultang on Scopolamine-Induced Memory Deficits in Mice

From text mining of Dongeuibogam, the 7 herbs in Palmultang can be considered effective candidates for memory enhancement. We sought to determine whether Gagam-Palmultang, comprising these 7 herbs, ameliorates scopolamine-induced memory impairment in mice, by focusing on the central cholinergic syst...

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Published in:Evidence-based complementary and alternative medicine 2018-01, Vol.2018 (2018), p.1-11
Main Authors: Baek, Jin Ung, Park, So Hyun, Pak, Malk Eun, Kwon, Min Young, Kim, Yu Ri, Choi, Byung Tae
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description From text mining of Dongeuibogam, the 7 herbs in Palmultang can be considered effective candidates for memory enhancement. We sought to determine whether Gagam-Palmultang, comprising these 7 herbs, ameliorates scopolamine-induced memory impairment in mice, by focusing on the central cholinergic system and memory-related signaling molecules. Behavioral tests were performed after inducing memory impairment by scopolamine administration. The cholinergic system activity and memory-related molecules were examined in the hippocampus by enzyme-linked immunosorbent, western blot, and immunofluorescence assays. Gagam-Palmultang ameliorated scopolamine-induced memory impairment in the Morris water maze test, producing a significant improvement in the mean time required to find the hidden platform. Treatment with Gagam-Palmultang reduced acetylcholinesterase activity and expression in the hippocampus induced by scopolamine. The diminished phosphorylated phosphatidylinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB), and mature brain-derived neurotrophic factor (mBDNF) expressions caused by scopolamine administration were attenuated by treatment with Gagam-Palmultang. This treatment also promoted neuronal cell proliferation in the hippocampus. Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway. Therefore, this multiherb formula may be a useful therapeutic agent for diseases associated with memory impairments.
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The diminished phosphorylated phosphatidylinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB), and mature brain-derived neurotrophic factor (mBDNF) expressions caused by scopolamine administration were attenuated by treatment with Gagam-Palmultang. This treatment also promoted neuronal cell proliferation in the hippocampus. Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway. 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The diminished phosphorylated phosphatidylinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB), and mature brain-derived neurotrophic factor (mBDNF) expressions caused by scopolamine administration were attenuated by treatment with Gagam-Palmultang. This treatment also promoted neuronal cell proliferation in the hippocampus. Gagam-Palmultang has beneficial effects against scopolamine-induced memory impairments, which are exerted via modulation of the cholinergic system as well as the PI3K and ERK/CREB/BDNF signaling pathway. 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subjects 1-Phosphatidylinositol 3-kinase
Acetylcholinesterase
Aging
Alzheimer's disease
Animal cognition
Brain-derived neurotrophic factor
Cell proliferation
Chemical compounds
Cholinergic transmission
Cognitive ability
Cyclic AMP response element-binding protein
Data mining
Dementia
Drug dosages
Enzymes
Ethylenediaminetetraacetic acid
Extracellular signal-regulated kinase
Herbal medicine
Herbs
Hippocampus
Immunofluorescence
Immunoglobulins
Impairment
Kinases
Medicine
Memory
Mine wastes
Neurogenesis
Neurosciences
Protein binding
Proteins
Rodents
Scopolamine
Signal transduction
title Beneficial Effects of Gagam-Palmultang on Scopolamine-Induced Memory Deficits in Mice
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