🧬 BDNF Extraction Viewer

Извлечено: 997 / 997 (100.0%) Средняя confidence: 0.13
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Lucidenic acid A drives PI3K/AKT/BDNF signaling to improve memory impairment in mice and alleviate cellular nerve damage.

PMID: 41453549 · DOI: 10.1016/j.jep.2025.121099 · Journal of ethnopharmacology, 2026 · Yichen Xie, Fusheng Gao, Ying Geng, Weijia Chen, Jia Zhou, Jianan Geng, Zhongmei He
📄 Abstract

Enhancing memory and alleviating amnesia are among the conditions that Ganoderma lucidum has historically been used to treat. However, there are relatively few studies on the potential therapeutic effects of active ingredients derived from Ganoderma lucidum in the treatment of memory impairment. This study investigated the ameliorative effect of Lucidenic acid A (LAA) on memory impairment via in vivo and in vitro experiments using experimental pharmacology approaches. In vivo, behavioral tests were used to evaluate memory impairment in mice. Transmission electron microscopy, Hematoxylin-Eosin (HE) staining, and Nissl staining were employed to observe pathological changes in mice. Western blotting (WB) was used for protein expression analysis. In vitro, CCK-8 assay and cell scratch test were used to evaluate changes in cell viability. Reactive oxygen species (ROS) immunofluorescence staining was used to assess intracellular oxidative stress changes. WB was also used for protein expression analysis. The results show that LAA can not only improve spatial learning and memory abilities and alleviate cholinergic system impairments in mice with memory impairment, but also mitigate oxidative stress and inflammatory responses, and reduce pathological changes in brain tissue. In addition to improving memory impairment in mice, LAA can also alleviate inflammation, oxidative stress, and neuronal apoptosis induced in cells. LAA can induce the activation of the PI3K/AKT/BDNF pathway, thereby alleviating inflammation, oxidative stress, and cholinergic system impairments caused by scopolamine (SCOP) administration, and improving memory impairment.

Confidence: 0.2 · 10 полей извлечено
Идентификация (6 полей)
Target
0.00
Alt. target
0.00
Protein family
0.00
Functional class
0.00
Subcellular loc.
0.00
Isoforms (metab/obesity)
0.00
Механизм действия (21 полей)
Mechanism
Lucidenic acid A activates PI3K/AKT/BDNF signaling pathway
0.95
Mutations (obesity/lean)
0.00
Activity (obesity)
0.00
Activity temporal
0.00
Energy balance
0.00
Appetite
0.00
Fat metabolism
0.00
Lipolysis
0.00
Thermogenesis
0.00
Muscle metabolism
0.00
Inflammation
Lucidenic acid A alleviates inflammation
0.90
Glucose metabolism
0.00
AA metabolism
0.00
Hormonal pathways
0.00
Cell death
Lucidenic acid A alleviates neuronal apoptosis
0.90
Adipocyte fibrosis
0.00
Upstream (biochem)
0.00
Upstream (physiol)
0.00
Downstream (biochem)
BDNF
0.90
Downstream (physiol)
0.00
PTMs
0.00
Экспрессия (8 полей)
Tissue expression
0.00
In vitro
CCK-8 assay, cell scratch test, ROS immunofluorescence staining, Western blotting
0.90
In vivo
behavioral tests, transmission electron microscopy, HE staining, Nissl staining, Western blotting
0.90
In silico
0.00
Genetic association
0.00
Ex vivo
0.00
Animal model
mice with memory impairment induced by scopolamine
0.90
Diet/model
0.00
Клиника (11 полей)
Drug
Lucidenic acid A
1.00
Indication
memory impairment
0.90
Patient subgroups
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Safety concerns
0.00
Off-target
0.00
Trial stage
0.00
Pharma competitors
0.00
AE severity
0.00
MOA weight loss
0.00
Endpoints
0.00
Approved
False
0.80