<i>Aster glehni</i>Extract Ameliorates Scopolamine-Induced Cognitive Impairment in Mice

Liao, Yulan; Bae, Ho Jung; Park, Jong‐Hun; Zhang, Jiabao; Koo, Bo-Kyung; Lim, Mi Kyung; Han, Eun Hye; Lee, Sang Ho; Lew, Jae Hwan; Ryu, Jong Hoon

doi:10.1089/jmf.2018.4302

Cited by 16 publications

(12 citation statements)

References 56 publications

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“…Regarding the utilization of A. glehni, several studies have concentrated on its pharmacological and therapeutic effects on diverse diseases [17][18][19][20][21]. Recently, it has been reported that ethanolic extract of A. glehni has ameliorating effects on scopolamine-induced memory dysfunction including longterm or working memory and improves memory function [22]. According to the study, its effects are due to the inhibition of acetylcholinesterase activity and the activation of ERK-CREB-BDNF and PI3K-Akt-GSK-3β pathways [22,23].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been reported that ethanolic extract of A. glehni has ameliorating effects on scopolamine-induced memory dysfunction including longterm or working memory and improves memory function [22]. According to the study, its effects are due to the inhibition of acetylcholinesterase activity and the activation of ERK-CREB-BDNF and PI3K-Akt-GSK-3β pathways [22,23]. However, further application of A. glehni in herbal medicine or functional food has been limited as there is inadequate knowledge of its safety.…”

Section: Discussionmentioning

confidence: 99%

“…glehni contains caffeoylquinic acid (CQ) derivatives such as 3,5-di-O-caffeoylquinic acid (3,5-DCQA), 5-O-caffeoylquinic acid, 3-O-caffeoylquinic acid, and 3-O-pcoumaroylquinic acid and flavonoids such as astragalin and kaempferol [18,21]. According to recent research, ethanolic extract of A. glehni (EAG) and 3,5-DCQA have ameliorating effects on memory impairment caused by scopolamine in male ICR mice [22,23]. It has also been reported that 3,5-DCQA inhibits the activity of acetylcholinesterase (AChE) and amyloid-beta (Aβ) induced cytotoxicity in SH-SY5Y neuroblastoma cells [23][24][25].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Subchronic Toxicity and Genotoxicity of Ethanolic Extract of Aster glehni Leaves and Stems

Lim

Yoon²,

Jeong³

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Aster glehni, a traditional plant on Ulleung Island in the Republic of Korea, has been recognized for its multiple medicinal properties. However, potential toxicity and safety analyses of A. glehni have not been previously investigated. Therefore, this study aimed to evaluate the safety profile of ethanolic extract of A. glehni leaves and stems (EAG) in terms of genotoxicity and subchronic oral animal toxicity under OECD guidelines and GLP conditions. Toxicological assessments were performed at doses of 1,250, 2,500, and 5,000 mg/kg/day in a 13-week oral repeated-dose toxicity study of EAG in male and female SD rats. In addition, an Ames test, an in vitro mammalian chromosomal aberration test, and a micronucleus test were performed. No toxicological changes in clinical signs, body weights, water and food consumption, urinalysis, hematology, clinical biochemistry, gross findings, and histopathological examinations were observed in subchronic oral animal toxicity. In addition, EAG gave negative results when evaluated using in vitro and in vivo genotoxicity tests. In conclusion, the no-observed-adverse-effect level (NOAEL) of EAG was considered to be 5,000 mg/kg/day, and no target organs were identified in both sexes of rats. EAG was also classified as nonmutagenic and nonclastogenic in genotoxicity testing. Collectively, these results show a lack of general toxicity and genotoxicity for EAG that supports clinical work for development as a herbal medicine.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evaluation of Subchronic Toxicity and Genotoxicity of Ethanolic Extract of Aster glehni Leaves and Stems

Lim

Yoon²,

Jeong³

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…We observed an improvement in BDNF levels, a neurotrophic factor widely distributed in the central nervous system, in the hippocampus along with the ameliorative hippocampus-dependent cognitive function in CX3CR1-deficient mice after SD, which is the opposite of the WT group. BDNF is one of the most important regulators of synaptic plasticity, closely related to cognitive function [25]. It has been confirmed to modulate ligand-gated channels like N-methyl-D-aspartic acid (NMDA) and α-amino-3hydroxy-5-methyl-4-isoxazole-propionicacid (AMPA) receptors.…”

Section: Discussionmentioning

confidence: 99%

CX3CR1 modulates cognitive dysfunction induced by sleep deprivation

Xin¹,

Cheng²,

Xie³

et al. 2020

Preprint

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Background Sleep disorder-associated cognitive impairments are often accompanied by impaired synaptic plasticity. In the pathological process of sleep deprivation, microglia, as an important innate immune cell in central nervous system, are involved and mediate the synaptic pruning, in which the CX3C-chemokine receptor 1 receptor (CX3CR1) plays an indispensable role. In this study, the potential role of CX3CR1 in modulating the cognition decline during sleep deprivation was evaluated in terms of microglial neuroinflammation and synaptic pruning. Methods Middle-aged wild type C57BL/6 mice (WT) (13 months) and age-matched CX3CR1 -/- mice were either subjected to sleep deprivation (SD) or allowed normal sleep (S) for 8 h to mimic the pathophysiological changes of middle-aged people after staying up all night in real life. The hippocampus-dependent cognition was assessed by fear conditioning test. Mice brains were extracted for neuroinflammation and synaptic pruning studies. Data were analyzed by Student’s t-test and one-way analysis of variance (one-way ANOVA). Results The CX3CR1 deficiency mice differed from WT mice in many measures. CX3CR1 deficiency prevented SD-induced cognitive impairments, in which the levels of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP-responsive element binding protein (p-CREB) were markedly increased in the hippocampus. Compared with the CX3CR1 -/- -S group, the CX3CR1 -/- -SD mice reported a markedly decreased microglial density in the dentate gyrus, notably-decreased levels of cellular oncogene fos (c-fos), and pro-inflammatory cytokines and increased levels of anti-inflammatory cytokines in the hippocampus, and a significant increase in the density of spines of the dentate gyrus area. Furthermore, the CX3CR1 -/- -SD group also showed a decreasing expression of microglial phagocytosis-related factors. Conclusion These findings suggest that CX3CR1 deficiency leads to different cerebral behaviors and responses to sleep deprivation. CX3CR1 deletion can alleviate the sleep deprivation-induced cognitive impairment. The inflammation-attenuating activity and the related modification of synaptic pruning are possible mechanism candidates, which indicate CX3CR1 as a candidate therapeutic target for the prevention of the sleep loss-induced cognitive impairments.

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“…or piracetam (200 mg·kg −1 , i.p.) as a positive control 1 hr before the acquisition trial, as previously described (Liao et al, 2019). When the mice entered the non‐illuminated chamber, the door was closed and a sub‐effective electroshock (3 s, 0.25 mA) was delivered to the mice through the stainless steel rods.…”

Section: Methodsmentioning

confidence: 99%

The effect of maslinic acid on cognitive dysfunction induced by cholinergic blockade in mice

Bae

Kim

et al. 2020

British J Pharmacology

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Background and Purpose: Alzheimer's disease (AD) is the most prevalent disease associated with cognitive dysfunction. Current AD therapeutic agents have several gastrointestinal or psychological adverse effects and therefore, novel therapeutic agents with fewer adverse effects must be developed. Previously, we demonstrated that oleanolic acid, which is similar in chemical structure to maslinic acid, ameliorates cognitive impairment through the activation of tropomyosin receptor kinase (TrkB)-ERK-cAMP response element-binding protein (CREB) phosphorylation and increased levels of brain-derived neurotrophic factor (BDNF). In the present study, we investigate the effect of maslinic acid on cholinergic blockade-induced memory impairment in mice. Methods and Key Results: Maslinic acid reversed scopolamine-induced memory impairment, as determined by the Y-maze, passive avoidance and Morris water maze tests. In addition, we also observed that ERK-CREB, PI3K and PKB (Akt) phosphorylation levels were increased by maslinic acid administration in the mouse hippocampus. Moreover, we determined that the effects of maslinic acid on scopolamine-induced memory impairment in the passive avoidance test were abolished by a specific TrkB receptor antagonist (ANA-12). Additionally, we observed similar temporal changes in the expression levels between BDNF and tissue plasminogen activator in the hippocampus. Conclusion and Implications: These findings suggest that maslinic acid enhances cognitive function through the activation of BDNF and its downstream pathway signalling in the hippocampus and that it might be a potential therapeutic agent for cognitive decline, such as that observed in AD. 1 | INTRODUCTION Alzheimer's disease (AD) is the most prevalent cause of dementia, which is related to ageing and cognitive dysfunction (Bishop, Lu, & Yankner, 2010; Samanez-Larkin & Knutson, 2015). The accumulation of polymerized β-amyloid (Aβ) monomers or the phosphorylation of tau protein, resulting in the formation of amyloid plaques or neurofibrillary tangles that induce neuronal cell death, is observed in AD

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Aster glehniExtract Ameliorates Scopolamine-Induced Cognitive Impairment in Mice

Cited by 16 publications

References 56 publications

Evaluation of Subchronic Toxicity and Genotoxicity of Ethanolic Extract of Aster glehni Leaves and Stems

Evaluation of Subchronic Toxicity and Genotoxicity of Ethanolic Extract of Aster glehni Leaves and Stems

CX3CR1 modulates cognitive dysfunction induced by sleep deprivation

The effect of maslinic acid on cognitive dysfunction induced by cholinergic blockade in mice

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