AI Article Synopsis
- This study investigates how Astragaloside IV affects astrocyte senescence caused by amyloid-beta, a key factor in aging and neurodegenerative diseases.
- It finds that Astragaloside IV reduces senescence markers and increases neurotrophic growth factors, which may help in protecting brain cells from degeneration.
- The research highlights hsp90aa1 as a potential target for Astragaloside IV, suggesting that manipulating this protein could lead to new treatment strategies for age-related neurological conditions.
Article Abstract
Cell senescence is intensively related to aging and neurodegenerative diseases. This study aimed to explore the effect and targets of Astragaloside IV against amyloid-beta-induced astrocyte senescence. Oligomerized amyloid-beta was prepared to culture with human astrocytes. The effects of Astragaloside IV were assessed based on SA-β-gal staining analysis, senescence markers (p53, p16INK4, and p21WAF1), neurotrophic growth factor levels (qRT-PCR), and cell proliferation (CCK-8 kit). The targets for Astragaloside IV were predicted, and hsp90aa1 protein was verified using molecular docking. After hsp90aa1 overexpression, the effects of Astragaloside IV on amyloid-beta-induced astrocytes were assessed. Treatment of human amyloid-beta-induced astrocytes with Astragaloside IV can decrease the percentage of SA-β-gal positive cells, downregulate the p53, p16INK4, and p21WAF1 levels, and increase the levels of neurotrophic growth factors (IGF-1 and NGF mRNA) and cell proliferation. Based on target prediction, hsp90aa1 was found to be a potential target of Astragaloside IV. Moreover, cellular experiments demonstrated that exogenously enhanced expression of hsp90aa1 overexpression suppressed the protective effect of Astragaloside IV on amyloid-beta-induced human astrocytes. The results presented here demonstrate that Astragaloside IV could confront amyloid-beta-induced astrocyte senescence via hsp90aa1, possibly opening new therapeutic avenues.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.32725/jab.2024.015 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The compound (E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one alleviates neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease.
Neural Regen Res
November 2025
Department of Medicinal Chemistry, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian Province, China.
JOURNAL/nrgr/04.03/01300535-202511000-00034/figure1/v/2024-12-20T164640Z/r/image-tiff Previous studies have shown that the compound (E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one (D30), a pyromeconic acid derivative, possesses antioxidant and anti-inflammatory properties, inhibits amyloid-β aggregation, and alleviates scopolamine-induced cognitive impairment, similar to the phase III clinical drug resveratrol. In this study, we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology.
View Article and Find Full Text PDFAmyloid beta-induced signalling in leptomeningeal cells and its impact on astrocyte response.
Mol Cell Biochem
November 2024
School of Engineering, Bernal Institute, University of Limerick, Limerick, Ireland.
The pathological signature of Alzheimer's disease (AD) includes the accumulation of toxic protein aggregates, mainly consisting of amyloid beta (Aβ). Recent strides in fundamental research underscore the pivotal role of waste clearance mechanisms in the brain suggesting it may be an early indication of early onset AD. This study delves into the involvement of leptomeningeal cells (LMCs), crucial components forming integral barriers within the clearance system, in the context of AD.
View Article and Find Full Text PDFAstragaloside IV confronts amyloid-beta-induced astrocyte senescence via hsp90aa1.
J Appl Biomed
September 2024
Xiangyang Hospital of Traditional Chinese Medicine (Xiangyang Institute of Traditional Chinese Medicine), Department of Anesthesiology, Xiangyang 441000, China.
Article Synopsis
- This study investigates how Astragaloside IV affects astrocyte senescence caused by amyloid-beta, a key factor in aging and neurodegenerative diseases.
- It finds that Astragaloside IV reduces senescence markers and increases neurotrophic growth factors, which may help in protecting brain cells from degeneration.
- The research highlights hsp90aa1 as a potential target for Astragaloside IV, suggesting that manipulating this protein could lead to new treatment strategies for age-related neurological conditions.
Quercetin ameliorates neuroinflammatory and neurodegenerative biomarkers in the brain and improves neurobehavioral parameters in a repeated intranasal amyloid-beta exposed model of Alzheimer's disease.
Food Funct
August 2024
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER) - Raebareli, Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow-226002, Uttar Pradesh, India.
: The aim of the present study was to study the potential therapeutic effects of quercetin in protection against repeated intranasal exposure of an amyloid-beta-induced mouse model. : Mice received intranasal Aβ (5 μg/10 μL) exposure once daily for seven consecutive days. Quercetin was orally administered to them at 30 mg kg and 100 mg kg doses for one week starting from day five following Aβ peptide administration.
View Article and Find Full Text PDFInhibition of Sphingosine Kinase 1 Reduces Sphingosine-1-Phosphate and Exacerbates Amyloid-Beta-Induced Neuronal Cell Death in Mixed-Glial-Cell Culture.
Neurol Int
July 2024
Laboratory of Integrative Physiology in Veterinary Sciences, Osaka Metropolitan University, Izumisano 598-8531, Osaka, Japan.
In Alzheimer's disease (AD) pathology, the accumulation of amyloid-beta (Aβ), a main component of senile plaques, activates glial cells and causes neuroinflammation. Excessive neuroinflammation results in neuronal dropouts and finally produces the symptoms of AD. Recent studies suggest that disorder in sphingosine-1-phosphate (S1P) metabolism, especially the decreased expression of sphingosine kinase (SK)1, followed by the reduction in the amount of S1P, can be a promotive factor in AD onset.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!