ArticlePloS one2014
Loading into nanoparticles improves quercetin's efficacy in preventing neuroinflammation induced by oxysterols.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 109 citations in OpenAlex.
- Enzymatic Nanomotors Integrated with Plant Extracts: Biochemical Mechanisms, Applications, and Clinical Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Oxysterol signaling in the central nervous system: cellular mechanisms and implications for neurodegeneration.Frontiers in molecular neuroscience · 2026Review
- Identification of Key Biomarkers Related to Lipid Metabolism in Acute Pancreatitis and Their Regulatory Mechanisms Based on Bioinformatics and Machine Learning.Biomedicines · 2025Article
- Oxysterol-Induced Inflammation in Human Diseases: Strategies for Treatment with Natural Compounds and Synthetic Molecules.Molecules (Basel, Switzerland) · 2025Review
- Targeting signaling pathways in neurodegenerative diseases: Quercetin's cellular and molecular mechanisms for neuroprotection.Animal models and experimental medicine · 2025Review
- Anti-inflammatory potential of quercetin: From chemistry and mechanistic insight to nanoformulations.Current research in pharmacology and drug discovery · 2025Review
- Green synthesis of nanoparticles using medicinal plants as an eco-friendly and therapeutic potential approach for neurodegenerative diseases: a comprehensive review.Frontiers in neuroscience · 2024Review
- Nanoparticle-delivered quercetin exhibits enhanced efficacy in eliminating iron-overloaded senescent chondrocytes.Nanomedicine (London, England) · 2024Article
- Regulation of cellular senescence by innate immunity.Biophysics reports · 2023Article
- Therapeutic potential of natural products in inflammation: underlying molecular mechanisms, clinical outcomes, technological advances, and future perspectives.Inflammopharmacology · 2023Review
- Polyherbal and Multimodal Treatments: Kaempferol- and Quercetin-Rich Herbs Alleviate Symptoms of Alzheimer's Disease.Biology · 2023Review
- Quercetin-1,2,3-Triazole Hybrids as Multifunctional Anti-Alzheimer's Agents.Molecules (Basel, Switzerland) · 2023Article
- Polyphenols and Their Impact on the Prevention of Neurodegenerative Diseases and Development.Nutrients · 2023Review
- Anti-Inflammatory Effects of Dietary Polyphenols through Inhibitory Activity against Metalloproteinases.Molecules (Basel, Switzerland) · 2023Review
- Molecular basis for the recognition of 24-(S)-hydroxycholesterol by integrin αvβ3.Scientific reports · 2023Article
- Lignan-Rich Sesame (Antioxidants (Basel, Switzerland) · 2023Article
- Plant-Based Antioxidants for Prevention and Treatment of Neurodegenerative Diseases: Phytotherapeutic Potential ofAntioxidants (Basel, Switzerland) · 2023Review
- Identification of Side Chain Oxidized Sterols as Novel Liver X Receptor Agonists with Therapeutic Potential in the Treatment of Cardiovascular and Neurodegenerative Diseases.International journal of molecular sciences · 2023Article
- Influence of the Neuroprotective Properties of Quercetin on Regeneration and Functional Recovery of the Nervous System.Antioxidants (Basel, Switzerland) · 2023Review
- A Flavonoid on the Brain: Quercetin as a Potential Therapeutic Agent in Central Nervous System Disorders.Life (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammatory events appear to play a fundamental role in Alzheimer's disease (AD)-related neuropathological changes, and to result in neuronal dysfunction and death. The inflammatory responses observed in the AD brain include activation and proliferation of glial cells, together with up-regulation of inflammatory mediators and of free radicals. Along with glial cells, neurons themselves can also react and contribute to neuroinflammatory changes in the AD brain, by serving as sources of inflammatory mediators. Because excess cholesterol cannot be degraded in the brain, it must be excreted from that organ as cholesterol oxidation products (oxysterols), in order to prevent its accumulation. Among risk factors for this neurodegenerative disease, a mechanistic link between altered cholesterol metabolism and AD has been suggested; oxysterols appear to be the missing linkers between the two, because of their neurotoxic effects. This study shows that 24-hydroxycholesterol, 27-hydroxycholesterol, and 7β-hydroxycholesterol, the three oxysterols potentially implicated in AD pathogenesis, induce some pro-inflammatory mediator expression in human neuroblastoma SH-SY5Y cells, via Toll-like receptor-4/cyclooxygenase-2/membrane bound prostaglandin E synthase (TLR4/COX-2/mPGES-1); this clearly indicates that oxysterols may promote neuroinflammatory changes in AD. To confirm this evidence, cells were incubated with the anti-inflammatory flavonoid quercetin; remarkably, its anti-inflammatory effects in SH-SY5Y cells were enhanced when it was loaded into β-cyclodextrin-dodecylcarbonate nanoparticles, versus cells pretreated with free quercetin. The goal of loading quercetin into nanoparticles was to improve its permeation across the blood-brain barrier into the brain, and its bioavailability to reach target cells. The findings show that this drug delivery system might be a new therapeutic strategy for preventing or reducing AD progression.
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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.