ReferenceID 5678

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

Br J Pharmacol

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 there

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Reference Id
5678
Evidence Id
22268
Core Evidence Id
22268
Source Reference Id
4600
Herb2 Reference Id
HBREF005397
Subject Paper Key
HBIN034527_32133639
Pubmed Id
32133639
Doi
10.1111/bph.15042
Paper Title
The effect of maslinic acid on cognitive dysfunction induced by cholinergic blockade in mice
Paper Abstract
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.
Journal
Br J Pharmacol
Publish Year
2020
Experiment Subject
mouse
Experiment Type
Animal Experiment
Phenotype Related
Alzheimer's Disease; Cognitive Impairment; Cognitive Dysfunction; Cognitive Decline
Paper Title Cn
Paper Title En
The effect of maslinic acid on cognitive dysfunction induced by cholinergic blockade in mice
Bilingual Status
semi_complete