ArticleMolecular neurobiology2024
Alisol A Exerts Neuroprotective Effects Against HFD-Induced Pathological Brain Aging via the SIRT3-NF-κB/MAPK Pathway.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Alisols A-C and their acetate derivatives: a review of natural occurrence, pharmacology, semisynthesis, pharmacokinetics, and metabolism.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Alisol A Mitigates Neuroinflammation and Oxidative Stress After Subarachnoid Hemorrhage Through SIRT3-Driven Reprogramming of Mitochondrial Metabolism.Molecular neurobiology · 2026Article
- From mitochondrial oxidative stress to neuroinflammation: integrated proteomic and transcriptomic profiling reveals the role of the ROS/TXNIP/NLRP3 signaling pathway in anxious depression.Frontiers in immunology · 2026Article
- SIRT3 deficiency exacerbates cognitive decline by disrupting mitochondrial antioxidant homeostasis in D-galactose-induced aging mice.Journal of translational medicine · 2025Article
- Identification and Therapeutic Potential of Polymethoxylated Flavones inMolecules (Basel, Switzerland) · 2025Article
- Alisol A Exerts Anti-Proliferative Activity against Human Oral Cancer Cells through Triggering JNK/p38 MAPK-Mediated Apoptotic Cascade.Oncology research · 2025Article
- Alisol A ameliorates vascular cognitive impairment via AMPK/NAMPT/SIRT1-mediated regulation of cholesterol and autophagy.Theranostics · 2025Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Chronic consumption of a high-fat diet (HFD) has profound effects on brain aging, which is mainly characterized by cognitive decline, inflammatory responses, and neurovascular damage. Alisol A (AA) is a triterpenoid with therapeutic potential for metabolic diseases, but whether it has a neuroprotective effect against brain aging caused by a HFD has not been investigated. Six-month-old male C57BL6/J mice were exposed to a HFD with or without AA treatment for 12 weeks. Behavioral tasks were used to assess the cognitive abilities of the mice. Neuroinflammation and changes in neurovascular structure in the brains were examined. We further assessed the mechanism by which AA exerts neuroprotective effects against HFD-induced pathological brain aging in vitro and in vivo. Behavioral tests showed that cognitive function was improved in AA-treated animals. AA treatment reduced microglia activation and inflammatory cytokine release induced by a HFD. Furthermore, AA treatment increased the number of hippocampal neurons, the density of dendritic spines, and the expression of tight junction proteins. We also demonstrated that AA attenuated microglial activation by targeting the SIRT3-NF-κB/MAPK pathway and ameliorated microglial activation-induced tight junction degeneration in endothelial cells and apoptosis in hippocampal neurons. The results of this study show that AA may be a promising agent for the treatment of HFD-induced brain aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.